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Néphrologie – Urologie Partie I – Module 5 – Q 55 (1/2)
Andropause Dr Sylvie SALENAVE1, Dr Stéphane
DROUPY2,3, Pr Jacques YOUNG1,3
1. Service d’endocrinologie et des maladies maladies de la reproduction 2. Service d’urologie d’urologie 3. Groupe d’étude des infertilités infertilités et d’andrologie de Paris XI CHU de Bicêtre, Bicêtre, Université Paris Sud 94 275 Le Kremlin-Bicêtre Cedex
[email protected] jacques.young@bc t.ap-hop-paris.fr
Points Forts à comprendre • La testostér testostérone one totale totale (TT) mesurée mesurée circul circulee majoritairement sous forme liée (98 %), principalement à la SHBG sex hormone-binding globulin). ( sex • La testostérone totale diminue avec l’âge tandis que la SHBG augmente. La testost érone libre (TL), qui refléterait mieux l’imprégnation androg énique de l’organisme diminue alors d’autant plus. Ainsi à 75 ans, la testostérone totale diminue diminue de 30 % et la testostérone libre de 60% 60 % par rapport aux taux observés à l’âge de 30 ans. • Les mécanismes (testiculaire et [ou] hypothalamo-hypophysaire) responsables ne sont pas clairement élucidés. • Devant cette baisse modérée de testostérone totale est préf éré le terme plus appropri é de déficit androgénique partiel de l’homme âgé plutôt qu’andropause.
epuis une dizaine d ’ann ées, on a pu observer un intérêt croissant pour les études traitant des modifications des hormones sexuelles chez les hommes âgées. Celui-ci tient au vieillissement naturel de la population avec une augmentation tr ès importante des sujets de plus 75 ans dans les pays dits d éveloppés. Ainsi, le nombre d ’Am éricains de plus de 65 ans qui était de 3,1 millions en 1900 est pass é à 34 millions ! À ces considérations démographiques il faut ajouter des
D
que les malades atteints d’un hypogonadisme classique. Quoi qu’il en soit, l’état de santé et le bien-être de cette population, jadis marginale, sont devenus logiquement une priorité. La décroissance d’un certain nombre d’hormones avec l’âge a fait soulever l’hypothèse de l’existence l’existen ce de « déficits hormonaux hormonaux » chez les sujets sujets âgés qui pourraient être responsables au moins d’une partie de la morbidité liée à l’âge. Le traitement substitutif de ces «carences « carences hormonales » devenait devenait à l’ordre du jour. C’est dans ce contexte que le thème de l’« andropause » s’est développé au cours de ces dernières années. Il est très difficile de schématiser un domaine de la médecine où il existe si peu de certitudes. Concernant l’andropause la seule démonstration qui a été faite à ce jour est celle cel le d’une diminution modérée et progressive de la testostérone plasmatique avec l’âge. Mais la signification de cette baisse reste peu claire. Nous ne savons pas, en effet, si cette décroissance est un simple phénomène adaptatif ou s’il participe à la morbidité liée à l’âge. De même il n’existe pas de certitude permettant d’affirmer que la correction correction de cet « hypogonadism hypogonadismee » par une androgénothérapie permettra de prévenir ou d’améliorer certains effets de la sénescence. Enfin les effets secondaires d’un traitement prolongé par les androgènes des hommes âgés n’ont pas été évalués sur des effectifs et une durée suffisants. DÉFINITION La ménopause est définie chez la femme par l ’épuisement du capital folliculaire ovarien. Celui-ci a 2 cons équences : d’une part une infertilité et d’autre part un arrêt complet des sécrétions hormonales ovariennes. Chez l ’homme, il n’y a pas d’interruption brutale de la spermatogenèse ni effondrement des s écrétions hormonales testiculaires. Comme nous l’avons évoqué, seule existe une diminution modérée et progressive de la s écrétion de testostérone qui rend impropre le terme d’andropause et fait préf érer celui, plus adapté à la réalité, de d éficit androgénique partiel de l’homme âgé (PADAM pour partial andr androgenic ogenic deficit in aging males).
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ANDROPAUSE
Évolution des concentrations avec l’âge Libre Testost érone totale Fraction { Libre – 2 2 % libre
}
Fraction non Liée liée à l’albumine à la 68 % SHBG
Liée à la SHBG 30 % Normal
}
Fraction liée à la SHBG
Liée à l’albumine Libre
Plusieurs études transversales et longitudinales ont montré une diminution de la testost érone circulante avec l’âge, même si on sélectionne des sujets en bonne sant é. La testostérone totale commence à décro î tre tre de façon linéaire chez le sujet normal vers la trentaine (fig. 2). La vitesse de d écroissance à été estim ée à 0,4 % pour la testostérone totale et de 1,2 % pour la testostérone libre, par an, chez l’homme sain. À chaque tranche d ’âge, les hommes âgés, atteints d’une maladie chronique, ont des valeurs de 10 à 15 % inf érieures.
Liée Liée SHBG
à l’albumine
50
à la
) L / l o m n ( e n o r é t s o t s e T
Liée à la SHBG
SHBH élevée hyperthyro ï die die administration d’œstrogènes déficit en androgènes cirrhose mitotane
SHBH basse hypothyro ï die die obésité acromégalie
1
Diff é rentes fractions de la testost é rone circulante chez l ’ homme homme normal et au cours des é tats pathologiques modi fiant la concentration de la protéine porteuse sex hormonebinding globulin (SHBG)
affinité appelée SHBG (sex hormone-binding globulin) autrefois appel ée TeBG TeBG et 60 % est lié faiblement à l’albumine. Moins de 2 % de la testost érone totale circule librement. Les mesures habituelles de testost érone concernent la testostérone totale (TT) c’est-à-dire la somme des formes liées et libres. Les dosages de la testost érone libre (TL) ou dialysable sont une estimation de la testost érone non liée aux protéines. On pense que cette fraction refl è te mieux l’imprégnation androgénique de l’organisme. Les seules techniques fiables font appel à une technique de dialyse non utilisée en routine. À leur place de nombreux laboratoires ont mis au point des kits de dosage de testost érone libre qui ne sont pas fiables et conduisent très souvent à
r 2 = 0,11
p < 0,001
40 30 20 10 0 20
40
60
80
Âge (années)
2
Évolution Évolu tion de la test testosté ostérone rone tota totale le plas plasmati matique que en fonction de l’âge. Parallèlement à cette baisse, la concentration de SHBG augmente (fig. 3) de ce fait la testost érone libre et la testostérone biodisponible diminue plus que la testost érone totale. Ainsi d’après certaines études, à 75 ans la testostérone totale moyenne le matin diminue de 30 % par rapport rapport aux concentrations observées entre entre 20 et 30 ans ans alors que les taux moyens des fractions biodisponibles et libres ne représentent que 40 % de ce qu ’ils é taient chez les hommes jeunes.
300 250 ) L / l o m n (
200 150
r 2 = 0,13
p < 0,001
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Néphrologie – Urologie Urologie
MÉCA CANI NISM SMES ES DE L’ANDROPAUSE Il existe, chez les hommes âgés, une tendance à l’augmentation de la LH (luteinizing hormone) plasmatique ainsi qu’une diminution modérée de la réponse testiculaire à l’administration d’hCG (human chorionic gonadotrophin ) ayant fait évoquer une atteinte de la fonction leydigienne. Cette hypothèse a été renforcée par l’observation d’une diminution des cellules de Leydig avec l’â ge. À cette atteinte testiculaire primitive semble s’ajouter un déficit gonadotrope partiel se traduisant par une élévation insuffisante de la LH en regard de la baisse de la testost érone plasmatique, par une r éponse atténuée des gonadotrophines à la GnRH ( gonadotrophin-releasing hormone) exogène et par une att é nuation du rythme nycthéméral du couple LH-testost érone. Pour certains, il existerait même une diminution de la bioactivité de la LH circulante.
DIA IAGNO GNOSTI STIC C D’HYPOGONADISME CHEZ L’HOMME ÂGÉ Il n’existe pas encore de définition consensuelle de l’hypogonadisme chez l ’homme âgé. Chez le sujet jeune, le diagnostic est établi pose lorsque la testost érone totale circulante est en dessous de 2 d éviations standard par rapport à la moyenne des hommes d ’âge comparable. En pratiqu prat ique, e, le diagnostic est consid considéré lorsque la concentration de testost érone totale est inf érieure à 3 ng/mL (< 2,5 DS) et il devient tr è s probable en dessous de 2 ng/mL. Chez le sujet âgé la testostérone totale moyenne étant plus basse, la limite inf érieure de la normale devrait l’être aussi. Malheureuse Malheureusement ment les normes données par les labora laboratoires toires ne tiennent pas compte des variations li ées à l ’âge et les chiffres donn és correspondent aux valeurs normales des hommes jeunes.
Testostérone inf érieure à 2 ng/mL En pratique, lorsque la testost érone totale chez un homme âgé, a priori en bonne sant é, est inf érieure à 2 ng/mL, le diagnostic d’hypogonadisme est probable. Il faut dans ce cas localiser le niveau, hypothalamohypophysaire ou testiculaire en dosant les gonadotrophines plasmatiques FSH ( foll follicle icle-sti -stimula mula ting hormone) et LH. Une élévation, en particulier de FSH, émoigne d’une atteinte testiculaire primitive alors
Testostérone entre 2 et 3 ng/mL La situation est moins simple lorsque la testost érone totale est comprise entre 2 et 3 ng/mL. Ici, 4 éventualités sont à envisager. Tout d’abord il peut s’agir d’une baisse partielle liée à l’âge qui serait relativisée par l’existence de normes adapt ées à l ’âge du sujet. En deuxième lieu, il est souhaitable de v érifier s’il existe une maladie chronique ou des prises m édicamenteuses pouvant retentir sur le fonctionnement gonadique. La troisiè me possibilité est celle d ’un chiffre bas par le simple fait que le prélèvement a été effectué au moment d’un nadir de la sécrétion de testostérone qui est pulsatile. Dans ce cas un deuxième prélèvement, à r éaliser systématiquement, montrant un chiffre normal permet d ’écarter un hypogonadisme. Finalement, un chiffre de testost érone totale compris dans cet intervalle peut t émoigner d’un hypogonadisme d ébutant ce qui nous ram ène à la situation précédente. Trancher entre ces 4 possibilit és est un v éritable dé fi quotidien pour l’endocrinologue. C’est dans ce cas que le dosage de la testost érone biodisponible et de la SHBG peut être utile montrant par exemple une baisse de cette protéine porteuse, responsable d ’une baisse art éfactuelle de la testost érone totale avec une testostérone biodisponible normale, ce qui est fr é quent chez les malades obèses ou ayant une hypothyro ïdie. À ce stade, nous devons r épéter que, compte tenu de la sous-estimation tr ès fr équente de la testost érone libre circulante par les kits du commerce, ce type de dosage qui risque de déclencher une épidémie d’hyp hypogo ogonad nadism ismes es ne peut être recommandé.
CONSÉQU QUEN ENCE CES S DE LA DI DIMI MINU NUTI TION ON DE LA TE TEST STOS OST TÉRONE
Chez l’homme avec un hypogonadisme « vrai » Les signes cliniques d ’appel d ’un hypogonadisme acquis après la pubert é résultent d’une diminution de l’imprégnation de l ’organisme par la testost érone et l’estradiol. Du point de vue comportemental, on observe une diminution de la force vitale et de la sensation de bien-être, de l’agressivit é, de l’activité et surtout de la libido, qui peut parfois s’accompagner d ’un dysfonctionnement érectile. Au niveau somatique, lorsque le déficit androgénique est partiel, une gynécomastie peut
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ANDROPAUSE
responsable d ’une accumulation de masse grasse en particulier au niveau abdominal qui, associ ée à la perte musculaire, serait responsable d ’insulinorésistance. Finalement la carence en testost érone sévère, par le déficit en estradiol qu’il entra î ne, ne, est responsable d ’une diminution de la masse min érale osseuse et donc d ’une ostéoporose. Chez un patient ayant un hypogonadisme certain, authentifi é par une exploration hormonale, l’ensemble de ces signes cliniques est corr élé à l’importance du déficit en st éroïdes sexuels. Surtout ce qui caract érise ces anomalies est leur r égression, souvent spectaculaire, après administration d’un traitement substitutif androgénique ce qui permet d ’établir facilement une relation de cause à effet entre la baisse de la testost érone plasmatique constaté e et les plaintes du malade et (ou) les signes cliniques observ és.
Chez le sujet âgé La situation est beaucoup plus complexe chez les sujets âgés. Certes, les signes cliniques ci-dessus voient leur pr évalence augmenter avec l ’â ge ce qui rapproche au plan sémiologique le sujet âgé des patients ayant un hypogonadi hypog onadisme sme postpost-pubert pubertaire. aire. Cependant, bien qu’un certain nombre d’é tudes aient mis en évidence une corrélation entre ces signes d ’hypogonadisme (tableau I) et les taux de testost érone circulante, l’analyse de la litt érature médicale consacr ée à ce sujet est pour l ’instant plutôt contradictoire, ce qui empêche d’établir une relation de causalit é formelle entre la baisse de la testost érone avec l’âge et ces signes d ’hypogonadisme. Par ailleurs, il faut garder à l ’esprit que la plupart des symptômes li és à l’â ge sont multifactoriels et que d’autres facteurs hormonaux (d é ficit en hormone de croissance et en androg ènes surrénaux) ou des paramètres non endocriniens (morbidité associ ée, prises m édica-
TRAITEMENT Androgénothérapie chez le sujet âgé Les objectifs proclamés par les partisans d’une androgénothérapie chez les sujets âgés sont de ramener les concentrations de testostérone totale aux valeurs normales des sujets jeunes, de soulager les sympt ômes pouvant être en rapport avec une carence androgénique, de maintenir ou améliorer la qualité de vie des hommes âgés et, si possible, de prévenir certaines affections pouvant être favorisées par le déficit en testostérone.
Résultats des essais thérapeutiques publiés Avant de résumer les effets de ta testost érone chez les hommes âgés, il faut rappeler que les résultats publiés reposent sur un nombre r é duit d’essais contr ôlés ne totalisant que quelques dizaines ou centaines de sujets et dont la durée est limitée. Comme on le voit, ces échantillons sont très en deçà des dizaines de milliers de femmes qui ont été incluses dans les études à long terme ayant permis d’éclaircir les effets du traitement substitutif de la ménopause. La solidité des preuves actuellement apport ées est donc limitée ce qui doit conduire à une grande prudence. Sch ématiquement, ces études semblent montrer que l’administration de testostérone à des sujets âgés ayant une baisse de la testostérone a un effet bénéfique sur l’humeur, la libido et la sensation de bien- être. Au plan somatique, une augmentation de la masse et de la force musculaires et une baisse de la masse grasse abdominale ont aussi été rapportées. En outre, un effet bénéfique sur les marqueurs de remodelage et sur la densit é m min inérale osseuse a été décrit. La plupart de ces effets sont modestes et certains d’entre eux ne sont pas retrouv és par tous les auteurs. Il est aussi int éressant de noter que certains de ces effets sont d’autant plus significatifs que la baisse initiale de la testostérone est importante.
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Néphrologie – Urologie Urologie
TABLEAU II
Médicaments utilisés en androgénothérapie Dénomination commune internationale (DCI) ❚ ❚ ❚ ❚
Heptylate de testostérone rone ne Énanthate de testostéro Undécanoate de testostérone Testostérone gel 2%
Nom
Présentation
retiré Androt Andr otar ardy dyll Pantestone Androgel
ampoul ampo ulee 25 250 0 mg comprimé 4 40 0 mg sachet 50 mg
––
de la simplicité et du prix dans la mesure où une injection intramusculaire assure une couverture de 3 à 4 semaines à t trrès faible coût. Son inconvénient théorique est d’induire la 1re semaine des concentrations plasmatiques supraphysiologiques de testost érone qui pourraient majorer les effets secondaires de ce st éroïde. Depuis le retrait de la vente de l’hepty heptylate late de testos testosttérone, le seul représentant est l’énanthate de testostérone (Androtardyl). La dose préconisée en cas d’hypogonadisme est d’une injection inject ion IM de 250 mg toutes toutes les 3 à 4 semaines. Comme d’habitude un traitement par anticoagulants est une contre-indication à cette voie d’administration. La voie orale est possible gr âce à l’utilisation de l’undécanoate de testost érone (Pantestone). Sa demi-vie courte rend nécessaire la prise de 3 capsules à 40 mg par jour. Bien que minoré par un passage lymphatique, le m étabolisme hépatique explique la faible élévation de la testostérone plasmatique et l ’augmentation plus importante de la dihydrotestostérone. Depuis environ 1 an, on peut administrer la testost érone par voie percutanée grâce à un gel contenant le st éroïde naturel non estérifié. La dose habituelle est un sachet de 50 mg (Androgel) que le patient étale sur la peau chaque matin. L’avantage théorique de ce produit est l’absence de pic supraphysiologique de testost érone mais l’observance à long terme d’une application quotidienne (hors protocole) n’est pas d étermin ée. Cependant, son co ût
Posologie
––
250 25 0 mg mg/3 /3 à 4 se sem 40 mg x 3/j 51 mg/j
Administration
Prix
Sécurité sociale
––
––
––
intramusculaire per os percutanée
1,91 � /ampoule 17,71 � /60 cp 69,87 � /30 sachets
65 % 65 % 0%
La survenue ou l’aggravation d’apnées du sommeil induites par la testostérone sont discutées ; il s’agit donc d’une contreindication très relative ne se posant pas souvent en pratique. L’hépatotoxicité des diff érentes voies d’administration de testostérone semble marginale. Par contre celle-ci est non négligeable lorsqu’on utilise des androgènes 17-alkylés. L’apparition ou la majoration d’une gynécomastie est un effet secondaire fréquent du traitement par la testost érone du fait de son aromatisation en estradiol. Bien que souvent modérée, celle-ci peut parfois obliger à l’interruption du traitement ou conduire à l ’utilisation concomitante ou alternative de dihydrotestostérone par voie locale.
Alternatives à l’androgénothérapie En dehors des troubles sexuels du sujet âgé, pouvant être en rapport avec une carence androg énique, la justification du traitement par la testost érone s’appuie sur des effets positifs concernant des param ètres pour lesquels de nombreuses alternatives thérapeutiques existent. Il en est ainsi de l ’activité physique régulière qui permet de majorer la masse maigre et la fo rce musculaire ainsi que de diminuer la masse grasse et l ’insulinoré sistance. L’exercice physique associé à des règles hygiéno-diététiques est probablement au moins aussi efficace que la testostérone dan danss la prévention d’événements délétères liés au vieillissement. Concernant l ’ost éoporose, n’oublions pas que la carence vitamino-calcique du sujet âgé est un
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Pathologie de l’appareil locomoteur Partie I – Module 5 – Q 57
Arthrose Ar throse Pr Xavier CHEVALIER Service de rhumatologie Centre hospitalier Henri-Mondor 94010 Créteil
[email protected]
Points Forts à comprendre • L’arthr ’arthrose ose est une maladie maladie de l’articulati l’articulation on qui se caractérise par une destruction du cartilage. • C’est une une maladie maladie liée au vieillisse vieillissement ment mais dont l’origine est plurifactorielle. • L’horair ’horairee des douleurs douleurs est est mécanique. mécanique. • L’usur ’usuree progressiv progressivee du cartil cartilage age entraîne entraîne un handicap fonctionnel qui croît au fil du temps. • La radiographi radiographiee reflète reflète avec avec retard retard les modifications structurales. • Il n’y a pas pas de traiteme traitement nt médical médical curatif curatif de l’arthrose. • Le seul traiteme traitement nt radical radical est le remplac remplacement ement de l’articulation par une prothèse articulaire.
ÉPIDÉMIOLOGIE DESCRIPTIVE
L’arthrose est une maladie très fréquente dont la prévalence augmente avec l’âge: l’âge : 52 % des adultes de plus de 75 ans sont atteints d’au moins une localisation arthrosique. C’est un problème de santé publique (seconde cause d’invalidité après les maladies cardiovasculaires). Les 3 localisations les plus fréquentes sont : les articulations digitales, le genou, la hanche. La prévalence varie en fonction de la définition clinique, radiologique ou anatomique. Elle est répartie de façon égale avant l’âge de 50 ans entre hommes et femmes, puis prédomine chez la femme en raison de la fréquence de la gonarthrose : 35 % chez les femmes de plus de 65 ans (cohorte de suivi de Framingham). L’incidence de la maladie est mal connue : environ 2 pour 1 000 adultes par par an pour la gonarthrose et seulement de 0,5 pour 1 000 adultes par an pour la coxarthrose. On distingue : • l’arthrose primitive qui peut être monoarticulaire ou généralisée (d é finie par au moins 3 localisations localisations : pieds, mains et genoux, souvent associ ées à une arthrose du rachis cervical et lombaire) ;
L’
arthrose est une maladie de l ’articulation, caractérisée par une dégradation progressive du cartilage, associée à une ostéophytose marginale, des remaniements de l’os sous-chondral et une inflammation minime de la membrane synoviale. La maladie résulte le plus souvent d’un désordre biomécanique sur lequel se
arthrose secondaire qui peut être : post-t post-traumati raumatique, que, • l ’ arthrose congénitale (dysplasie), due à une maladie m étabolique (ochronose, hémochromatose, maladie de Wilson, maladie de Gaucher), endocrinienne (acrom é galie, hyperparathyroidie, hyperparathyro idie, diabète), causée par d épôts de microcristaux articulaires (chondrocalcinose, goutte, dépôts d’apatite), par maladie osseuse ou articulaire acquise, par neuroarthropathie, par arthropathies
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ARTHROSE
TABLEAU I
Facteurs de risque d ’arthrose Non génétiques ❚
âge
poids ❚ statut hormonal ❚ maladies acquises os/articulation ❚ chirurgie articulaire (ménisque) ❚
Génétiques
sexe ❚ race ❚ maladie du collagène ❚
Environnement
occupations physiques et professionnelles ❚ traumatisme ostéoarticulaire ❚ activités sportives et de loisir ❚
les obèses (indice de masse corporelle ou IMC 30) contre 10 % chez des non-obèses (IMC < 30). L’hyperostose vertébrale serait un facteur lié à l’arthrose du genou.
L’horaire est m écanique : douleur lors de la mise en charge, à l’effort (au début seulement après un certain temps de marche ou lors d ’efforts inhabituels) et cédant à l ’arrêt de celui-ci, calmée par le repos et ne r éveillant pas le malade la nuit. Cependant, le rythme et l ’intensité de la douleur peuvent varier au cours de l ’évolution de la maladie. raideur est caractérisée par un temps de d érouillage • La raideur matinal toujours court, en règle tardive dans le cours de la maladie et au début souvent limitée à certains mouvements et aux changements de position. ementt arti articula cula ire peut ê tre noté par le • L’é panch emen patient ayant constat é une augmentation du volume de son genou. • L’impotence fonctionnelle, d’importance variable, est la conséquence de la douleur et (ou) de la raideur et (ou) de la présence d’un épanchement. Le handicap porte sur des activités de la vie courante : marche (appré cier le p érim è tre de marche), station debout, montée et descente des escaliers, vie sexuelle. Il existe des indices algofonctionnels (adapt és à chaque groupe articulaire) qui permettent de mesurer ce handicap (v. Pour approfondir 1, 2, 3 et 4). 4). • Autres sympt ô ô mes : une tendinopathie de la patte d’oie est fréquente au cours de la gonarthrose f émoro-tibiale interne. Il n’y a ni altération de l’état général, ni fièvre.
Examen clinique Facteurs locaux Des traumatismes articulaires par m écanisme direct (chondropathie), ou indirect (lésion du ligament croisé au genou), la ménisectomie étendue, l’activité professionnelle comportant le port de charges ou des gestes répétés, et une activité sportive (en dehors de la traumatologie) si pratiquée à haut niveau (courses, les sports de balles et de saut) sont des des facteurs à prendre en compte.
Les articulations portantes doivent être examinées en 3 temps : en position debout debout ; lors de la marche ; en position couch ée. L’examen doit être comparatif et locorégional (articulations de voisinage). • En position debout on repère les défauts d’axe mécanique du membre inf érieur : soit dans le plan sagittal (recurvatum ou flexum) ; soit dans le plan frontal (surcharge interne en cas de genu varum [appr [app récié en position debout par la distance intercondylienne] ou externe en
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Pathologie de l’appareil locomoteur
impose la ponction pour en confirmer la nature m éca canique nique : moins de 1 500 cellules (en fait souvent < 1 000) dont moins de 50 % de polynucl polynucléaires. • Il faut appré cier toujours de fa ç on comparative les structur stru ctures es liga ligament ment aires du geno u (majeur pour les indications de la chirurgie préventive) et rechercher une amyotrophie du quadriceps. Tout examen articulaire doit comprendre la palpation des pouls et un examen g éné ral à la recherche de comorbidités.
Signes radiogra radiographiques phiques Dans 90 % des cas, la radiographie standard montre les signes cardinaux de la maladie, maladie, ce qui rend le diagnostic aisé. Il faut systématiquement demander des radiographies comparatives en charge pour les articulations des membres inf érieurs. L’examen radiographique du genou comprend : face en appui bipodal, rotation nulle, genoux en extension + appui monopod monopodal al ; profil profil ; défilé f émoro-patellaire à 30° de flexion ; schuss (face post éro-antérieur, en charge, à 30° de flexion) visualise le compartiment post érieur. Les signes cardinaux de l ’arthrose sont : • le pincement de l ’interligne localisé , toujours apprécié de façon comparative comparative ; • l ’ ost ost é ophyto ophytose se dite margina marginale le externe qui peut être isolée au début. De face l ’ostéophytose est marginale volontiers affrontée et (ou) localis ée sur les épines tibiales. Sur le profil elle est post érieure, en avant et en arrière du tibia tibia ; osté oscl é rose condensante de l ’ os os sous-chondral : • l ’ ost située de part et d’autre de l’interligne pincé ; • des gé odes en nombre et en taille variables, situées dans les zones d ’hyperpression. On cote l ’importance de l ’atteinte radiologique par la classification de Kellgren et Laurence (bas ée sur le pincement et les ost éophytes) ou par la mesure du pince-
symptomatolog tologie ie clinique clinique est évoca vocatrice: trice: la douleur • La symptoma siège à la face antérieure du genou et irradie vers le bas. Elle est déclenchée par toutes les man œuvres de mise en tension de la rotule contre la trochl ée : la descente descente plus que la montée des escaliers, la marche en terrain in égal, la station assise prolong ée, l ’accroupissement ou l ’agenouillement. Cela contraste avec l ’absence de douleur lors de la marche en terrain plat. Elle peut s ’accompagner de signes d’accrochage douloureux à la marche et d ’épisodes d’épanchement. • Signes d ’exa examen: men: la douleur est réveillée à l’extension contrariée de la jambe, à la pression de la rotule sur le genou fléchi, à la percussion de la rotule, à la manœuvre de rabot (frottement de la rotule contre la trochlée), à l’ascension contrariée de la rotule lors de la contraction du quadriceps (signe de Zohlen). • Les signe signess radiog radiograp raphiqu hiques es comprennent les incidences axiales à 30 ou 60° et les incidences de face et de profil des genoux en charge. Les incidences axiales mettent en évidence des signes d’arthrose dans le compartiment externe. La rotule est souvent translatée en dehors. • Prof il évolutif : il faut souligner la fréquence des formes asymptomatiques. L’évolution est très souvent capricieuse. Les douleurs d’abord intermittentes deviennent gênantes notamment lors de la pratique de la marche et des activités sportives. • Trai Traitement tement : il faut insister sur la rééducation isométrique des axes internes de fa çon à r éaxer la rotule et l’amaigrissement est imp ératif. Interdire la pratique de sports tels que le ski, la bicyclette et les marches prolong ées. En cas d ’impotence s évè re et rebelle on envisage la chirurgie. L’utilité des interventions qui visent à r éaxer la rotule n’est pas démontrée. La prothèse totale de la rotule donne de bons r ésultats en cas d ’atteinte isolée f émoro-rotulienne.
2. Poussée congestive d’arthrose f émoro-tibiale Elle est caractérisée par une recrudescence douloureuse
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ARTHROSE
Coxarthrose primitive Certaines singularités méritent d’être soulignées.
1. Signes cliniques
• Siè ge de la douleur : la localisation la plus sp écifique est le pli de l’aine, plus rarement le grand trochanter ou la fesse. Cette douleur peut irradier à la face antérieure de la cuisse ou en ant éro-interne, jusqu’au genou voire ne siéger qu’en regard du genou. Aussi toute douleur du genou doit amener à examiner systématiquement la hanche homolatérale. • Le handicap porte sur la marche et les mouvements de rotation : difficulté pour les patients à mettre des chaussettes, à enfiler un collant et à se laver les pieds. Il peut retentir sur la vie sexuelle. • L’examen clinique clinique : – en position debout, on recherche une boiterie de hanche, une attitude vicieuse en flexum de hanche ou en rotation externe ; – en position couch ée, la hanche est examin ée en décubitus dorsal complet et en d écubitus ventral pour coter les rotations. Les premiers mouvements limit és sont la rotation interne et l’abduction.
1
Coxarthrose supé rieu rieure re globale globale.. Pincemen Pincementt de l ’interligne associé à une osté oph associ ophyto ytose se marg margina inale le et et une une ost osté oco oconde ndensa nsation tion sous-chondrale. sous-chon drale.
Coxarthrose sur dysplasie L’objectif majeur, chez un sujet jeune, est de ne pas passer à c ôté d’un vice architectural de la hanche. La hanche devient symptomatique vers l ’âge de 30 ans. Sur une radiographie standard de face et de profil, la coxométrie permet de dépister les anomalies architecturales de la hanche (fig. 2).
2. Signes radiographiques L’examen radiographique de la hanche comprend 3 clichés : bassin debout de face avec les membres en rotation interne à 20 °, un faux profil de Lequesne de chaque hanche
V
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Pathologie de l’appareil locomoteur
est souvent associ ée à une obliquit é excessive du toit avec un angle HTE > 12 °. La coxarthrose est sup éroexterne avec géodes. • Les 2 anomalies sont souvent associées. La dysplasie de hanche rend rend compte de 40 % des coxarthroses. Elle est souvent bilat érale et asymétrique.
2. Dysplasie interne ou protrusion acétabulaire Elle ne représente que 5 % des causes de coxarthrose, se rencontre plus souvent chez la femme et est volontiers bilatérale. Le début est souvent plus tardif et l’évolution plus lente que pour une coxarthrose sup éro-externe. Le diagnostic peut être évident si la protrusion est importante (coxa profunda) ou mise en évidence par la position de ligne ac étabulaire (arrière-fond) qui déborde en dedans la ligne ilio-ischiatique. Le pincement est i nterne de face et post érieur de profil.
3. Coxa plana Séquelle d’ostéochondrite de l’enfance (garçon entre 5 et 10 ans) ou maladie de Leggs Perthes et Calv é. La fragmentation du noyau céphalique conduit à un aplatissement de celui-ci avec pour s équelle une déformation dite en béret basque de la tête f émorale à l’âge adulte.
1. Arthrose des articulations interphalangiennes Elle s’observe plus volontiers chez la femme, avec souvent un caractère familial et héréditaire. • Sympt ô ô mes : il s’agit de tum éfactions nodulaires, douloureuses ou développées à bas bruit, entra î nant nant des déformations importantes des interphalangiennes distales, nodules d ’Heberden puis des interphalangiennes proximales (nodosités de Bouchard). La d éformation est souvent responsable d ’une impotence fonctionnelle. Le pré judi judice ce esth étique est parfois le seul motif de consultation. Le diagnostic est clinique. Les radiographies sont inutiles devant des d éformations typiques. • Signes radiographiques : la radiographie montre un pincement de l ’interligne et surtout une ost éophytose lat é rale en berge, tr è s exubé rante, responsable des nodosités. • Prof il évolutif : il existe une addition des atteintes topographiques au fil du vieillissement. L’évolution est émaillée de poussées douloureuses. Certaines arthroses restent indolores.
2. Arthrose érosive des doigts
4. Coxa retorsa
• Signes cliniques : il s’agit de pouss ées congestives très douloureuses des interphalangiennes proximales ou
Séquelle d’une épiphysiolyse de l’adolescent, volontiers bilatérale, qui survient entre 10 et 16 ans, souvent chez les gar ons obèses. Le glissement de la t ête f émorale en
interphalangiennes distales, de rythme inflammatoire avec réveils nocturnes évoluant par poussées de plusieurs semaines.
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ARTHROSE
• Sympt ô ô mes : la douleur localisée à la racine du pouce et à la partie externe du poignet s ’associe, au fil du temps, à une maladresse et une difficulté à la préhension. La mobilisation de la trapézo-métacarpienne est douloureuse, elle est parfois limit ée en abduction. Il s ’installe progressivement une déformation en pouce adductus. • Signes radiographiques : l’articulation trapézo-métacarpienne est d ’abord atteinte, puis dans un second temps, la scapho-trap é zienne. L’atteinte isol ée de la scapho-trapézienne doit évoquer le diagnostic de chondrocalcinose. • Profil évolutif : il est marqué par des périodes douloureuses qui s ’amendent au prix d ’une diminution de la mobilité. La gêne r ésultante est alors faible, sauf en cas d’instabilité séquellaire.
Diagnostic diff érentiel Le diagnostic diff érentiel se pose dans diff érentes situations. Toute douleur articulaire avant 45 ans doit rendre circonspect quant au diagnostic d ’arthrose. • Affirmer qu’il s’ agit agit bien d ’une douleur de l ’ articu articulation lat ion : il peut s’agir d’une douleur projetée de la coxof émorale, d’une douleur projetée d’une irradiation radiculaire au membre inf érieur (cruralgie L4), d ’une tendinopathie d’insertion de voisinage ou bursites de voisinage, d’une tumeur osseuse ou fissure osseuse de
Les explorations complémentaires (scintigraphie osseuse, scanner et surtout imagerie par r ésonance magnétique [IRM]) revê tent tout leur int érê t pour dé pist pister er : une ostéonécrose épiphysaire piphysaire;; une fissure de l’os sous-chondral sous-chondral;; une algodystrophie. En l’absence d’arguments pour ces diagnostics, le diagnostic d’arthrose préradiologique est hautement probable chez un sujet de plus de 50 ans.
Profil évolutif L’é volution de l’arthrose est souvent tr è s variable à l’échelon individuel (bien en avertir le patient). Il est inutile de r épéter les radiographies en dehors de toute évolution symptomatique. On peut schématiser 3 types d’évolut volution ion possibles: une atteinte intermittente lente – la plus fr équente – ; une atteinte avec poussées congestives entrecoupées de phases de stabilité prolongées ; une atteinte avec chondrolyse chondrolyse rapide (moins (moins de 5 %). Le surpoids, le stade avancé de la maladie, et l ’existence d’une désaxation notable sont des facteurs de progression anatomique de la gonarthrose. Même à un stade avancé, la gêne fonctionnelle peut rester mineure avec conservation d ’un périm ètre de marche suffisant.
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Pathologie de l’appareil locomoteur
Le traitement médical est toujours de mise car l ’évolution de la maladie n ’est pas inéluctable et il existe une grande variabilit é dans l ’intensit é et le rythme des douleurs d’un patient à un autre. Il ne faut pas laisser passer l ’heure de la chirurgie, soit préventive visant à corriger un défaut d’axe soit curative de remplacement proth étique lorsque le traitement médical ne fait plus la preuve de son efficacit é.
Traitement non pharmacologique Diff érentes mesures sont à mettre en œuv uvre re : • maintien d ’une activité de marche marche ; articulation (éviter les • mesures de mé nagement de l ’ articulation marches et les stations debout prolong ées, le port de charges lourdes, notamment pour la coxarthrose ; port d’une canne du cot é controlatéral à la douleur douleur ; repos quotidien) quotidi en) ; • Mesur Mesures es hygi hygié no-dié té tiques (perte de poids impérative pour les gonarthroses; port de chaussures avec avec des semelles épaiss paisses) es) ; • port d ’une orthè se correctrice ; • réé ducation isomé trique et isotonique (maintien de la trophicité musculaire, et du jeu articulaire articulaire ; lutte contre les attitudes antalgiques vicieuses à visée antalgique) qui peut être menée dans le cadre de programme d’autorééducation.
(misoprostol 400 mg), ou oméprazole 20 (1 cp/j). Les nouveaux AINS anti-cyclo-oxygénase de type 2 ont un meilleur profil de tolérance digestive. Ces AINS exposent cependant aux mêmes risques d’effets secondaires extradigestifs : atteinte rénale (anurie par diminution de la filtration glomérulaire) ; notamment chez les patients âgés qui ont une co-prescription de diurétiques ou d’antihypertenseurs ou une insuffisance r énale ; atteinte cutanée : toxidermie rare, surtout avec les oxicams et la ph énylbutazone. Les anti-inflammatoires sté ro ïdiens (corticothérapie) par voie orale n’ont pas leur place dans le traitement de l’arthrose. • Les antalgiques de niveau 2 : tramadol (dose efficace de 200 à 400 mg) ou associations parac étamol codéine ou paracétamol dextropropoxyphène (2 à 6 cp). La tol érance digestive et les inconv énients mineurs (vigilance) de ces produits doivent être surveillés. antalgiquess de niveau 3 ne sont pas recommandés. • Les antalgique • Les traitements dits anti-arthrosiques à action lente : diac érhéine, dérivés d’avocat et de soja, chondro ïtines sulfates. Ils ont en commun un effet antalgique modeste retardé (de 3 à 6 semaines) et r émanent à l’arrêt. Leur effet chondroprotecteur est incertain (la diacerhéine a l’indication dans le ralentissement de la coxarthrose). Leur profil de tolérance est bon, en dehors de diarrh ée sous diacerhéine dans 25 à 30 % des cas. cas.
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ARTHROSE
Traitement chirurgical 1. Traitement conservateur Il vise à réaxer une articulation de fa çon à prévenir ou à ralentir l’évolution. • À la hanche : l’indication se pose chez un sujet encore jeune (< ( < 50 ans) souffrant d ’une coxarthrose débutante sur dysplasie et consultant pour une g êne encore modérée. Les modalités de cette chirurgie : but ée cotyloïdienne ou ost éotomie (ostéotomie de Chiari ou de varisation du col) sont affaire de spécialistes. g enou : l’indication concerne des arthroses uni• Au genou compartimentales, internes ou externes, (l ’atteinte f émoropatellaire radiologique ne constitue pas une contre indication à cette chirurgie), douloureuses, d ésax ées sans hyperlaxité ligamentaire, avant l’âge de 70 ans. Elle retarde en moyenne la mise en place d’une prothèse du genou et non pas de la hanche.
2. Traitement radical ou chirurgie prothétique L’indication de remplacement articulaire proth étique est dictée par l’importance de l’atteinte clinique, douleur et (ou) gêne fonctionnelle confrontée à une atteinte radiologique avancée. L’atteinte radiologique à elle seule ne permet pas de porter une telle indication. La durée de vie moyenne des proth èses est de l’ordre de 15 ans, aussi bien bien pour la hanche hanche que pour pour le genou. Néanmoins les difficultés de remise en place d’une seconde
L’indication est plus difficile et se discute au cas par cas : sujet entre 40 et 60 ans et handicap majeur ; coxarthrose dé jà très évoluée avec un vice architectural chez un sujet jeune ; coxart coxarthrose hrose primi primitive tive chez un sujet jeune sans vice architectural. • Prot Proth hè se du geno u : soit prothè se totale du genou (PTG) soit prothèse dite « unicompartimentale » (PUC). Les complications sont les m êmes que celles de la prothèse totale de hanche, le risque de thrombophlébite est plus élevé pour la chirurgie du genou. L’indication est fonction de la topographie et de l’étendue des lésio sions ns : – arthrose globale ou unicompartimentale mais très évoluée : prothèse totale du genou ; – arthrose unicompartimentale, chez un sujet âgé, sans défaut d’axe majeur, sans hyperlaxit é : prothèse unicompartimentale.
Traitement de l ’arthrose digitale traiteme tement nt mé dica dicall doit insi insister ster sur : le port • Le trai d’orthèses (nocturne) pour limiter les déformation formationss ; le recours aux infiltrations cortisoniques doit être limité. chirurgie gie de l'art l'arthrose hrose des inte interphal rphalangi angiennes ennes • La chirur doit être, par principe, dé conseill ée compte tenu du caract ère extensif et diffus de la maladie. On discute exceptionnellement (pré judice esthétique ou fonctionnel
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Pathologie de l’appareil locomoteur
Points Forts à retenir
arthrose tarso-m é tatarsienne touche la femme de • L’ arthrose 70 ans ; elle se traduit par par une douleur mécanique à l’appui et par la fr équence d’un conflit avec la face dorsale de la chaussure (tum éfaction dorsale exubérante au niveau de la 1re cunéo-métatarsienne).
• Dans 90 % des cas, la douleur mécanique s’associe à une radiographie typique
2. Coude
•
L’arthrose du coude est rare, le plus souvent post-traumatique. Elle est caractéristique par la fréquence des ostéochondromes et le risque d’une compression du nerf ulnaire.
•
3. Épaule L’omarthrose est le plus souvent secondaire à une rupture de coiffe : elle est dite excentrée par ascension de la t ête hum é rale (diminution de l ’espace acromio-hum éral). Elle est plus rarement primitive. L’omarthrose est responsable de douleurs, de craquements et d ’une limi-
• •
ce qui rend la diagnostic facile. Il n’y pas de corrélation entre l’importance des douleurs et l ’importance de l’atteinte radiologique. Le diagnostic diff érentiel se pose essentiellement dans les formes débutantes devant une douleur mécanique à radiographie normale. Le profil évolutif est variable à l’échelon individuel. Le traitement est avant m édical et comprend des mesures non pharmacologiques associé à un traitement antalgique
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ARTHROSE
POUR APPROFONDIR APPROFONDIR (SUITE) Difficult és de la vie quotidienne Monter un étage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0 à 2 Descendre un étage. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0 à 2 Vous accroupir complètement . . . . . . . . . . . . . . . . . . . . . . . . . . . 0 à 2 Marcher en terrain irrégulier . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0 à 2 0 : aucun aucunee difficult difficult é 0,5 : peti petite te difficult difficult é 1 : diffi difficile cile 1,5 1, 5 : tr ès difficile TOT TO TAL . . . . . . . 2 : impo impossib ssible le
4 / Womac : autoquestionnaire Womac douleur Womac douleur Quelle est l’importance de la douleur… Aucune 0
Minime 1
Modér ée 2
Sévère 3
Tr ès sévère 4
lorsque vous marchez sur une surface plane ?
lorsque vous montez ou descendez les escaliers ?
3 / Indice fonctionnel de Lequesne dans la coxarthrose
la nuit lorsque vous êtes au lit ?
Douleur et gêne A – Nocturne
lorsque vous vous levez d ’une chaise ou que vous vous asseyez ?
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Gériatrie Partie I – Module 5 – Q 64
Autonom Au omie ie et dép épeendance chez le sujet âgé PR Alain FRANCO, DR Pascal COUTURIER Département Départem ent de médecin médecinee gériatrique et commun communautai autaire, re, CHU, 3804 38043, 3, Grenoble Cedex.
Points Forts à comprendre • Autonomi Autonomiee et dépendance dépendance ne ne s’opposent s’opposent pas mais se complètent pour appréhender la personne âgée dans sa globalité.
Analyse fonctionnelle des maladies Afin de distinguer les différents niveaux de retentissement de la maladie, l’OMS (Organisation mondiale de la Santé) a repris l’analyse fonctionnelle des maladies
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AUTONOMIE ET DÉPENDANCE CHEZ LE SUJET ÂGÉ
• Les signe signess fonction fonctionnels nels sont les chutes souvent prémonitoires, symptômes les plus fréquents, ainsi que l’incontinence urinaire, voire fécale. • Les signe signess psychi psychiques ques sont constants et dominent parfois le tableau en associant perte de l’initiative, de l’attention, de l’élan vital, de l’affect, crainte du lever et de la marche, clinophilie. Ce tableau constitue la régression psychomotrice. Les troubles cognitifs sont très fréquents, marqués par une confusion mentale souvent fluctuante, parfois associée à des troubles du comportement. • Les signes sociaux associent isolement progressif et négligence de l’entretien de la maison, puis de l’hygiène personnelle et vont conduire à l’épuisement des proches et de la famille. La conséquence en est la crise gérontologique et la demande d’hospitalisation urgente. L’ensemble de ces symptômes conduit au déclin fonc-
Évolution Conséquences de la d épendance sur la personne âgée
• Vie quotidienne : la dépendance retentit en premier lieu sur la vie quotidienne de la personne. Lorsque le maintien à domicile est possible, la dépendance impose la présence de personnes, ce qui n’est aisé ni à organiser, ni à accepter par la personne âgée. • Abandon du domicile : souvent nécessaire au profit de structures institutionnelles, le changement de lieu de vie doit être préparé avec la personne âgée, en élaborant progressivement un projet de vie qui intègre à la fois l’acceptation de la perte du domicile et la préparation au nouveau logement. • Vie affective : la dépendance influence la vie affective
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Gériatrie
une perte minimale d’information.
Évaluation de la dépendance Les outils d’évaluation utilisés dépendent des objectifs de l’évaluation. personne : lorsqu’une évaluation de la • Évaluer la personne dépendance concerne une personne donnée, elle vise les déficiences et les incapacités. Par exemple, évaluer la marche, c’est vérifier les troubles de l’équilibre et de la coordination (get up and go test , test de Tinetti). D’une manière générale, l’évaluation permet à une équipe médicale et soignante : de repérer les déficiences et incapacités qui retentissent retentissent sur l’environnement ; d’établir un plan de soins soins pour limiter limiter le handicap handicap;; de communiquer avec d’autres d’autres acteurs de santé; de suivre une même
repérables et coûteuses) représente une autre cible des enquêtes à l’échelle de la population. Outils d’évaluation
Les deux principales qualités recherchées pour un outil d’évaluation sont la validité et la reproductibilité. Une grille validée doit être utilisée en respectant les règles de recueil. On ne doit ni la modifier ni la panacher avec une autre. Parmi les outils validés, tout médecin doit pouvoir renseigner les plus couramment utilisés en France. 1. Dépendance pour les activités simples
La détermination des capacités d’un individu pour les gestes courants intéressant le corps utilisera l’échelle des activités de la vie quotidienne (AVQ) (AVQ) : soins corporels, habillement, toilette, transfert, continence, alimentation)
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A U TO N O M I E E T D É P E N D A N C E C H E Z L E S U J E T Â G É
dans la littérature internationale. Elle prédit de plus le pronostic en termes de morbidité et mortalité. 2. Dépendance pour les activités complexes
TABLEAU II
Échelle des activités instrumentales de la vie quotidienne (échelle de Lawton)
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Gériatrie
TABLEAU III
Grille AGGIR : les 10 variables discriminantes du modèle
de ces outils d’évaluation ressort de choix et de pratiques d’équipes spécialisées, notamment en gériatrie.
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A U TO N O M I E E T D É P E N D A N C E C H E Z L E S U J E T Â G É
autonomes, 50 décèdent dans un délai inférieur à 4 ans, 20 décèdent entre 4 et 6 ans et 20 entre 6 et 10 ans. Ce taux de réversibilité varie selon l’âge;; il est de 18 l’âge 18 % avant avant 80 ans et de de 4 % après. après. Ce taux de réversibilité varie selon les pathologies cau-
Points Forts à retenir • La dépendance d’un malade âgé représente la conséquence d’un état pathologique simple
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PARTIE I / MODULE VIEILLISSEMENT
Q
58
5
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VIEILLISSEMENT
Cataracte Tableau 2 CAUSES
Causes et types de cataractes TYPES
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Tableau
Traitements hormonaux
1 / ŒS TR O GÈ NE S Œstrogènes par voie orale 17 β-œstradiol
❚ ❚ ❚
Estrofem, Progynova Oromone, Provames Estréva
Œstrogènes conjugués équins
❚
Prémarin
Œstrogènes par voie percutanée (gels) 17 β-œstradiol
Œstrodose, Œstrogel, Estréva gel, Délidose ❚
Œstrogènes par dispositif transdermique (patch) 17 β-œstradiol
❚ ❚ ❚ ❚ ❚ ❚
Estraderm TTS Climara, Estradiol G Gam Femsept, Estrapatch Ménorest, Dermestril Thaïs, Systen Evafilm, Thaïs Sept
Œstrogènes par voie nasale
❚
Aerodiol
Discordance entre les études d’observation et les études prospectives : alors que les résultats attendus (à partir des études
d’observation) pour l’effet préventif du THS sur les conséquences d’observation) de l’ostéoporose ou du cancer du côlon ont été vérifiés par les études prospectives d’intervention, cela n’est pas le cas pour la prévention des événements cardiovasculaires et des troubles cognitifs. Quelles en sont les raisons ? Dans les études d’observation (où l’on analyse le devenir de cohortes de femmes « tout-venant »), les femmes spontanément traitées par les œstrogènes par leur médecin sont, en fait, avant même tout traitement, moins à risque cardiovasculaire (les médecins tendent à mettre aux œstrogènes des femmes qui fument moins, sont plus minces, font plus d’exercice, ont un meilleur niveau socio-éducatif...) que les femmes à qui leur médecin médec in a préféré ne pas en donner (biais de prescription). Certains effets délétères du THS s’expliquent peut-être par l’effet prothrombotique des œstrogènes qui ont pu favoriser la survenue d’accidents thrombotiques sur une pathologie coronarienne préexistante, chez certaines femmes prédisposées. Le type et la voie d’administration des œstrogènes jouent peut-être un rôle.
RISQUES 1. Cancer du sein
prévention secondaire. D’autre part, les œstrogènes ont un effet bénéfique connu sur le métabolisme lipidique (augmentation du HDL-cholestérol), sur la plaque d’athérome, sur l’endothélium vasculaire et favorisent la vasodilatation. Cependant, récemment, plusieurs études prospectives randomisées, contrôlées, contre placebo, menées à large échelle aux États-Unis (HERS, WHI), n’ont pas confirmé cet effet bénéfique du THS sur la survenue des événements cardiovasculaires, cardiovasculaires, et cela ni en prévention primaire ni en prévention secondaire. Au contraire, contraire, certaines études de prévention secondaire des maladies cardiovasculaires par le THS tendraient même à montrer une augmentation des événements, dans la première année ann ée de traitement (effet prothrombotique des œstrogènes oraux ?). Prévention des troubles cognitifs : un autre objectif longtemps revendiqué du THS était la prévention des troubles cognitifs, et en particulier de la démence. En effet, selon les études épidémiologiques d’observation, le THS prévenait la détéri oration cognitive, au moins en prévention primaire (moins de femmes sous THS développaient une maladie d’Alzheimer) mais non en prévention secondaire (en cas de maladie d’Alzheimer, le THS n’empêchait pas la détérioration). Cependant, d’après les résultats très récents des premières
Son risque de survenue est corrélé à la durée du traitement et à l’âge. Il est, en moyenne, augmenté de 20 à 30 % par le THS selon les études d’observation (comparant (comparant utilisatrices et non-utilisatrices non-utilisat rices de THS) ou les études prospectives d’intervention (comparant des femmes prenant un THS et des femmes prenant un placebo). En chiffres absolus, à l’échelon individuel, le risque reste minime. Ainsi, sur 10 000 femmes ne n e prenant pas d’œstrogènes, 450 auront un cancer du sein entre 50 et 70 ans (ce risque augmentant avec l’âge), alors que sous THS pendant 5 ans, le nombre de cas supplémentaires, pour 10 000 femmes est de 8 cas chaque année. À l’échelon d’une population comme celle de la Grande-Bretagne, selon la Million Women Study , le THS aurait néanmoins été à l’origine de 20 000 cas supplémentaires de cancer du sein durant les 10 dernières années.
2 / PR O GE ST AT IF S Progestérone naturelle et assimilés par voie orale
Utrogestan, Progestérone Biogaran, Biogar an, Ev Evapa apause use ❚ Estima ❚ Duphaston ❚
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VIEILLISSEMENT
Ménopause
3 / ŒS TR O GÈ NE S E T PR O GE ST AT IF S CO MB IN ÉS
Le risque de cancer du sein serait aussi (voire plus) important en cas d’association œstrogènes et progœstatifs qu’en cas d’œstrogènes seuls. Ce risque disparaît après l’arrêt du THS.
Voie orale 17 β-œstradiol...
et dydrogestérone et acétate de cyprotérone
❚ ❚ ❚ ❚ ❚ ❚ ❚ ❚ ❚ ❚ ❚
Naemis Climodière Avadène Successia Divina Duova Kliogest Activelle Trisequens Climaston Climène
Voie percutanée
❚
Femseptcombi
et acétate de nomégestrol et dienogest 17 β-œstradiol et gestodène
2. Accidents veineux thrombo-emboliques (AVTE)
et médroxypr médroxyprogestérone ogestérone
Le risque est multiplié par 2. En chiffres absolus, le risque r isque reste reste néanmoins minime : ainsi, si sur 5 années, pour 1 000 femmes non traitées par THS, 3 feront un AVTE entre 50 et 59 ans et 11 en feront un entre 60 et 69 ans, ces chiffres passent à 7 chez les femmes de 50-59 ans traitées par THS pendant 5 ans (4 AVTE en plus) et à 20 (9 AVTE en plus) chez les femmes de 60-69 ans traitées par THS pendant 5 ans. Ce risque paraît limité au THS oral.
et acétate de noréthistérone
AUTRES : Livial (tibolone)
3. Accidents vasculaires cérébraux (AVC) Le risque (AVC ischémiques mais non des accidents hémorragiques) pourrait être augmenté de 30 %.
4. Lithiases biliaires Leur risque serait augmenté de 50 % environ par le THS.
En l’absence d’utérus (hystérectomie), les œstrogènes peuvent être administrés seuls ; sinon, une association avec un progestatif (généralement administré de manière discontinue) est obligatoire afin de prévenir le risque d’hyperplasie de l’endomètre et donc de cancer de l’endomètre (tableau 2).
5. Balance bénéfices/risques en 2003
2. Progestatifs
En termes de risque absolu, il apparaît finalement que le THS donné pendant 5 ans à 1 000 femmes en bonne santé, dans des pays occidentaux, est responsable, soit d’un cancer du sein, soit d’un AVC, soit d’une embolie pulmonaire supplémentaire, chez 6 femmes de 50 à 59 ans et 12 femmes de 60 à 69 ans. Dans le même temps, pour 1 000 femmes âgées de 50 à 59 ans traitées par THS, 1,7 événement tel qu’un cancer colorectal ou une fracture du col fémoral est évité (5,5 pour 1 000 femmes de 60 à 69 ans traitées par THS). Quand on fait le bilan de tout cela, l’équilibre bénéfice/risque ne penche donc pas en faveur du THS.
Les produits utilisés habituellement sont la progestérone naturelle et les dérivés de la 17-hydroxyprogestérone, les norprégnanes et les prégnanes. Les progestatifs dérivés de la 19-nortestostérone doivent être évités (sauf en cas de mastopathie bénigne), compte tenu de leur effet androgénique délétère sur les paramètres métaboliques. En pratique, chez une femme souhaitant des hémorragies de privation (règles), ils sont administrés de manière discontinue (pendant 12 j, par exemple du 14e au 25e j). À l’in l’inver verse, se, chez les les femmes ne désirant pas de règles, on les administre en continu. On privilégie les schémas séquentiels (discontinus en progestatifs).
OYENS ENS THÉRA THÉRAPEUTI PEUTIQUES QUES MOY
CONTRE-INDICATIONS
1. Œstrogènes
1. Contre-indications absolues
En France, on utilise surtout l’œstrogène naturel, 17β-estradiol administré par voie orale, percutanée (gel), transdermique (patch) ou nasale (tableau). Les œstrogènes conjugués équins (Prémarin), les plus utilisés aux États-Unis (ceux des grandes études épidémiologiques) le sont moins en France. Administrés par voie percutanée ou transdermique on évite le premier passage hépatique des œstrogènes, ce qui limite l’augmentation l’augmentation des VLDL (very low density lipoprotein ) et des triglycérides. Inversement, on augmente moins le cholestérol-HDL. De même, ces voies d’ad-
Le cancer du sein est le cancer le plus fréquent fréquen t chez la femme. À plus
de 50 % des cas, cas, il survient après la ménopause. Le cancer cancer du sein est un cancer hormono-dépendant hormono-dépe ndant dont la prolifération est favorisée par les œstrogène œstrogènes. s. Il contre-indiq contre-indique ue formellement l’utilisation d’une œstrogénothérapie. Cette néoplasie doit être systématiquement éliminé éliminéee (examen (examen clinique, mammographie) avant toute prescription d’œstrogènes. d’œstrogènes. Les antécédents familiaux familiaux de cancer du sein, en particulier parmi les apparentés au premier degré (mère, sœur), peuvent constituer une contre-indication relative.
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probablement moins délétère que la voie orale dans la survenue d’événements thrombo-emboliques. Cela reste néanmoins à démontrer. Autres : hémorragie génitale sans diagnostic établi ; accident thrombo-embolique artériel récent ou en évolution ; affection hépatique aiguë ou chronique ; antécédents d’affection hépatique jusqu’à jus qu’à norm normalis alisatio ation n des tes tests ts hépa hépatiqu tiques es (en cas de pris prisee ora orale le des œstrogènes).
3. Indications En pratique (selon la mise au point sur le traitement hormonal hor monal substitutif de la ménopause rédigé par l’Afssaps en décembre 2003) : Chez la femme présentant des troubles fonctionnels liés à la patien te le carence œstrogénique : un THS peut être instauré, si la patiente
souhaite, à la dose minimale efficace, tant que durent les symptômes. Dans cette indication, le bénéfice/risque du THS reste favorable favorable à court terme (moins de 5 ans). Chez la femme ménopausée ayant des facteurs de risque d’ostéoporose : qu’il existe ou non des troubles climatériques, un THS
2. Insuffisance coronaire Les résultats des études prospectives randomisées ont récemment remis en cause l’indication d’un THS en prévention primaire et en prévention secondaire de la maladie coronaire. L’existence d’un état thrombotique connu non encore traité par les anticoagulants constitue donc une contre-indication à la prescription d’un THS. La présence de facteurs de risque coronarien (diabète, tabagisme, HTA) doit amener à bien évaluer le rapport bénéfice/risque avant de prescrire un THS. S’ils sont sévères (HTA sévère, dyslipidémie sévère, diabète) ou s’ils sont modérés mais associés, le THS n’est pas indiqué (haut risque cardiovasculaire) tant que le haut risque persiste. À l’heure actuelle, il n’a pas été clairement établi que l’insuffisance coronaire avérée constituait maintenant une contreindication au THS, mais un principe de précaution s’impose néanmoins. Ainsi, en cas d’antécédent d’infarctus du myocarde, de maladie coronarienne ou d’accident vasculaire cérébral, il est recommandé de ne pas prescrire de THS.
INDICATIONS, MISE EN ROUTE ET SUIVI 1. Bilan clinique La prescription de THS est toujours précédée d’un interrogatoire et d’un examen clinique rigoureux. L’interrogatoire confirme la réalité r éalité de la ménopause ménopau se (aménorrhée accompagnée de bouffées de chaleur depuis plus de 1 an). Avant l’âge de 50 ans (surtout 45 ans), le diagnostic de la ménopause doit être confirmé par un dosage de FSH de façon à ne pas méconnaître une autre cause d’aménorrhée. L’interrogat L’interrogatoire oire évalue aussi l’existence de facteurs de risque cardiovasculaire (obésité, tabagisme, sédentarité, diabète, hyperlipidémie) et bien entendu d’accidents thrombo-emboliques veineux. On recherche aussi des antécédents personnels et familiaux de néoplasie mammaire ou endométriale. La patiente est informée des risques à court, à moyen et à long terme pouvant être induits par le THS. En fonction de son profil, on choisit la voie d’administration : orale ou percutanée. L’examen clinique mesure le poids, la pression artérielle, permet un examen gynécologique et une palpation des seins.
peut être administré après recherche de facteurs de risque d’ostéoporose et éventuellement mesure de la densité minérale osseuse (DMO). Les facteurs de risque classiques de l’ostéoporose chez la femme sont : ménopause précoce ou iatrogénique; antécédents de fractures non traumatiques à l’âge adulte chez la femme ou chez un parent au premier degré; masse adipeuse faible ; prise de certains médicaments (glucocorticoïdes); consommation de tabac et d’alcool ; déficit en calcium et vitamine D, certaines affections potentiellement inductrices d’ostéoporose (hypogonadisme, hyperthyroïdie, hyperparathyroïdie). Le THS doit être instauré, à la ménopause, le plus précocement possible. L’effet L’effet sur la DMO augmente a ugmente avec la dose d’œstrogène. La durée recommandée de traitement est d’environ 5 ans. Au-delà, il est difficile de formuler des recommandations, compte tenu du risque de survenue d’effets indésirables, en particulier celui du cancer du sein, qui est corrélé à la durée du traitement et à l’âge. En cas d’initiation du THS au début de la ménopause, le surrisque de cancer du sein reste faible avant la 5e année de traitement. Au-delà, ce risque doit être ê tre pris en compte. Il devient notable après 65 ans. La perte osseuse reprend à l’arrêt du traitement. Elle est identique à celle des femmes de même âge non traitées. Les traitements alternatifs (biphosphonates, raloxifène) manquent encore de recul sur leur utilisation au-delà de 5 ans. Chez la femme sans trouble fonctionnel et sans facteur de risque d’ostéoporose d’ostéopor ose : le THS ne doit pas être prescrit de manière sys
tématique. Il doit être décidé au cas par cas, en fonction de la situation et des souhaits de la femme, en l’informant de l’ensemble des bénéfices attendus et des risques potentiels.
4. Surveillance et durée du traitement Après quelques mois de traitement, une nouvelle consultation en évalue la tolérance et l’efficacité (absence d’apparition d’une HTA, d’un diabète et d’une dyslipidémie) et vérifie le bon dosage des œstrogènes : une dose insuffisante se traduit par une persistance des bouffées de chaleur, éventuellement des autres
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VIEILLISSEMENT
Ménopause
ALTERNA TERNATIVES TIVES THÉRAPEUTIQUES Elles sont utiles en cas de contre-indications au THS classique. En cas d’ostéopénie, un traitement par les biphosphonates en association avec une thérapeutique vitamino-calcique peut être proposé (voir ostéoporose). Lorsque les bouffées de chaleur sont très symptomatiques, des traitements par la clonidine (Catapressan) ou des inhibiteurs spécifiques de la recapture de la sérotonine peuvent être essayés. Les modulateurs spécifiques du récepteur des œstrogènes (SERM) sont des molécules capables de se comporter compor ter comme un anti-œstrogène dans certains tissus-cibles et comme des œstrogènes sur d’autres. Le plus intéressant de cette famille est le raloxifène (Evista) qui mime les effets bénéfiques de l’œstradiol au niveau de l’os et du système cardiovasculaire, cardiovasculaire, mais se comporte comme un anti-œstrogène au niveau de l’endomètre et du sein. On peut donc concevoir une utilisation chez les femmes à risque de cancer du sein ou en alternance avec un THS classique, pour atténuer le risque de néoplasie né oplasie mammaire. Mais le raloxifène n’a pas d’effet sur les bouffées de chaleur et le tractus urogénital ; il a des effets prothrombotiques et son prix est actuellement élevé (il n’est pas pris en charge par l’Assurance maladie). La tibolone (Livial) est un composé stéroïdien de la famille de la 19-nortestostérone. Son action est à la fois œstrogénique, progestative et androgénique, selon l’action de ses métabolites sur les tissus-cibles (œstrogénique sur l’os et progestative sur l’endomètre). Elle améliore les bouffées de chaleur, la trophicité vaginale et la DMO. Le profil lipidique est moins favorable que sous œstrogènes (augmente les triglycérides et diminue le HDLcholstérol). Elle a un effet e ffet prothrombotique et a donc les mêmes contre-indications vasculaires que le THS. Son utilisation est simple (1 comprimé par jour). Sa tolérance est bonne. Le produit n’est pas pris en charge par l’Assurance maladie. On dispose de peu de données épidémiologiques à grande échelle concernant ce produit. Néanmoins, son utilisation serait associée à une augmentation de l’incidence du cancer du sein, comparable à celle des œstrogènes (Million Women Study publiée en 2003). Le cance cancerr du sein constitue donc une contre-indication contre-indication et
DEJÀ PARUS DANS LA REVUE
Traitement hormonal substitutif de la ménopause (THS) : recommandations ◗
Afssaps (Rev Prat Med Gen 2004 ; 18 [637-638] : 59-62) ◗
Ménopause
POINTS FORTS
à retenir
> La ménopause est un processus physiologique,
survenant vers 50 ans dont les conséquences (qu’on relie à la carence œstrogénique), sont, de longue date, considérées comme évitables par un traitement hormonal substitutif (THS) associant œstrogènes et progestatifs progestatifs..
> Les effets réels du THS ont été réévalués de façon
objective très récemment : à court-terme, il améliore le syndrome climatérique (et donc la qualité de vie en cas de bouffées de chaleur) ; à long-terme, il diminue la résorption osseuse et prévient les fractures (mais l’effet protecteur est limité à la période d’utilisation) ; il n’a pas d’effet bénéfique sur la survenue des événements cardiovasculaires (coronariens ou vasculaires cérébraux) tant en prévention primaire que secondaire, ni d’effet démontré sur la fonction cognitive.
> Le THS est associé à une augmentation de 20 à 30% de l’incidence du cancer du sein et à un doublement du risque d’accident veineux thrombo-embolique.
> Le rapport bénéfice/risque du THS doit donc être
discuté de façon individuelle et, si l’indication est retenue (après vérification des contre-indications), on recommande maintenant de proposer le THS pour 5-10 ans et l’on renforce par ailleurs les conseils hygiéno-diététiques (exercice (exercice physique, apport appor t vitamino-calcique).
> On utilise généralement l’estradiol-17 l’estradiol-17β, par voie orale
ou percutanée, 25 jours par mois (1er au 25e j), ass associ ociéé à un progestatif (progestérone naturelle, dérivés de la 17-hydroxy progestérone, norprégnanes ou prégnanes) durant 14 jours (14e au 25e j), le traitement étant ensuite interrompu pendant 3 à 7 jours.
(v. MINI TEST DE LECTURE, p. 1006) 1re partie : Andropause (parue : Rev Prat 2003 ; 53 [9] : 1015-9). 1015 -9).
justifie justif ie les mêm mêmes es con condit dition ionss de sur survei veillan llance ce mam mammai maire re que sou souss THS œstro-progestatif. Son effet sur le risque cardiovasculaire est inconnu. Finalement, chez une femme ménopausée ayant une contreindication aux œstrogènes, on n’oubliera pas le dépistage et la prise en charge des différents facteurs de risque cardiovasculaire, de façon à limiter la survenue d’événements cardiovasculaires
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Pathologie de l’appareil locomoteur Q 56
Ostéoporose PR Philippe ORCEL Fédération de rhumatologie, centre Viggo-Petersen, hôpital Lariboisière, 75475 Paris Cedex 10.
Points Forts à comprendre L’ostéoporose, éthymolo éthymologiquement giquement maladie des « os poreux poreux », est définie depuis depuis la confére conférence nce de consensus de Hong Kong de 1993 comme une «maladie « maladie diffuse diffuse du squelette, caractérisée par une diminution de la masse osseuse et une détérioration de la micro-ar micro-architecture chitecture trabéculairee osseuse, conduisant à une trabéculair une fragilité osseuse et à une augmentation du risque de fractur fract uree ». Cette définiti définition on «littéraire «littéraire » a pour intérêt de définir la maladie sur la base d’une fragilité osseuse et d’un risque fracturaire et non sur ses complications, complications, les fractures fractures ostéoporotiques. ostéoporotiqu es. Elle est peu utile en pratique clinique pour l’aide au diagnostic d’ostéoporose.
En 1994, un groupe de travail de l ’OMS (Organisation mondiale de la Sant é) a élabor é une d éfinition plus opérationnelle de l ’ostéoporose à partir de la mesure de la densit é min érale osseuse (DMO) par absorptiom étrie biphotoniquee à rayons X. Chez la femme m énopaus ée biphotoniqu caucasienne, l ’ostéoporose est d éfinie par une valeur de densité minérale osseuse inf érieure de plus de 2,5 écartstypes à la moyenne de la population normale d ’adultes jeuness de 20 à 30 ans (tableau I). Cette d éfiniti jeune finition on repo repose se sur des données é pid émiologiques solides corr élant la diminution de densit é minérale osseuse à l ’augmentation de l’incidence des fractures ost éoporotiques. Elle permet une d éfinition quantitative et reconna ît un état intermédiaire entre la normalit é et l’ostéopo oporose: rose: l’ostéopénie. Le seuil de d éfinition densitométrique de l’ostéoporose ne s’applique pas aux hommes ni aux patients sous corticoïdes, ni aux sujets de races non caucasiennes. Il ne doit pas être consid ér é comme un seuil d ’intervention thérapeutique systématique.
Données épidémiologiques Prévalence de l’ostéopor l’ostéoporose ose Avec le vieillissement, le nombre de femmes atteintes d’ostéoporose s’accroît s’accroît : à l’âge de la ménopause, seulement 15 % des femmes sont ostéoporotiques ostéoporotiques alors qu’à 80 ans cette proportion est est de 70 %. Soixante pour cent des femmes ostéoporotiques de 80 ans auront eu au moins une fracture. Sur 10 femmes caucasiennes arrivant à l’âge de la ménopause, 4 auront au moins une fracture ostéoporotique avant leur mort. Ce risque global est 3 fois inférieur chez les hommes. Risque de fracture L’augmentation du risque de fracture ost éoporotique est étroitement liée à la baisse de la densit é minérale osseuse. Une méta-analyse r écente a d émontr é que chaque diminution d ’un écart-type de densit é minérale osseuse multi pliait par 1,5 à 2,5 le risque de fracture de l ’extr émité supérieure du f émur (FESF), du poignet ou des vert è bres. Ce gradient de risque est tr ès similaire à celui qui existe entre l’élévation des chiffres de pression art érielle et le risque d ’accident vasculaire c ér é bral bral,, et sup érieur à celui qui lie l ’élévation de la concentration s érique de cholestérol et les coronaropathies ath éromateuses. La densité minérale osseuse n’est pas le seul d éterminant du risque de fracture. L’augmentation de la fragilit é osseuse est aussi sous la d é pendance d ’altérations de la qualit é d dee l ’os : perturbations de la micro-architecture du r éseau trabéculaire, modifications éventuelles de la minéralisation, caract éristiques géométriques des pièces osseuses (é paisseur des corticales et diam ètre des dia physes , long longueur ueur de l ’axe central du col f émoral…). L’impact de ces modifications qualitatives sur le risque de fracture reste mal connu. Les alt érations de la microarchitecture trab é culaire ne sont pas quantifiables en pratique clinique.
TABLEAU I
Définition densitométrique de l’ostéopo oporo rose, se, selo selon n l ’OMS
Facteurs de risque d’ostéoporose et de fractures
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O S T É O P ORO S E
TABLEAU II
Facteurs de risque d ’ostéoporose (densit é minérale osseuse basse) et de fracture ostéoporotique Facteurs de risque de densit é minérale osseuse basse ❑ « curables »
corticothérapie ; hypogonadisme; hypogonadisme; manque d ’exer exercice cice ; immobilisation immobilisatio n ; insuffisance calcique calcique ; carence en vitamine vitamine D ; tabac; tabac ; alcool; alcool ; pathologies pathologies ostéopéniantes ❑ « non curables » ménopause pr écoce; âge ; race (blanch (blanche, e, jaune) jaune) ; faible indice de masse corporelle corporelle ; pubert é tardive Facteurs de risque de fracture ost éoporotique ❑ « curables »
chutes fr équentes; troubles visuels visuels ; troubles de l’équil quilibre; ibre; sédatifs/h datifs/hypotenseu ypotenseurs rs ; obstacles ❑ « non curables » antécédent personnel de fracture avant avant 50 ans ; antécédent maternel de fracture du col f émoral ; faible indice de masse corporelle ; long axe du col f émoral
être l’objet d ’une intervention pr éventive ou thérapeutique spécifique (tableau (t ableau II). Il est donc tr ès important d ’identifier ces facteurs de risque au cours de l ’enquête clinique. Chez les sujets âgés, les chutes et leurs facteurs de risques risques sont particu part iculi lièrement associés au risque de fracture de l ’extr émité supérieure du f émur et doivent être cherchés et corr corrig igés.
Épidémiologie des fractures ostéoporotiques Les fractures ostéoporotiques peuvent toucher tous les os, hormis le cr âne, les vert è bres cervicales cer vicales et dorsales hautes, les mains et les orteils. Elles excluent les fractures traumatiques et surviennent spontan ément ou à l’occasion d ’un traumatisme mineur (incluant une chute de sa hauteur).
suivant la fracture) et de la morbidit é (pl (plus us de de 50 % de complications infectieuses, thrombo-emboliques et cutan ées). Elle est souvent responsable d ’une perte d ’autono autonomie mie : 30 à 50 % des patientes doivent recourir à une tierce personne ou être admises en institution de long s é jour. Elle génère des coûts de santé consid érables, évalués à pr ès d ’un demi-milliard d ’euros par an en France. L’é pid émiologie des fractures vert é brales (improprement (improprement appelées « tassements verté brau braux x ») est moins bien connue, car pr ès de deux tiers d ’entre elles seraient asymptomatiques. La pr évalence des fractures vert é brales (FV) est évaluée essentiellement à partir de radiographies du rachis r éalisées chez des sujets repr ésentant des échantillons de population, s électionnés pour les grands essais th érapeutiques. Les crit ères morphologiques et (ou) morphométriques de d éfinition de la fracture vert é brale ne sont pas standardisés. L’incidence des fractures vert é brale braless augmente progressivement avec l ’âge, dans les 2 sexes, mais les fractures vert é brale braless sont plus fr équentes chez les femmes que chez les hommes entre 60 et 80 ans. La survenue d ’une fracture verté bral bralee augmente augmente consid consid érablement le risque d ’autres fractures vert é brales dans l’année qui suit (phénomène appelé « cascade des fractures »). Les manifestations cliniques des fractures vert é brales sont : les douleurs rachidiennes chroniques ; la perte perte de taille; taille ; la d éformation en cyphose ; l’augmentation du handicap (impotence fonctionnelle, difficult és respiratoires liées aux d éformations thoraciques et digestives li ées à la ptose abdominale) ; le retentissement psychologique psychologique des d éformations et de la perte de taille. L’é lévation de la mortalité est mod ér ée et plus progressive que pour les fractures de l ’extr émité supérieure du f émur. La fracture de l ’avant-bras ou du poignet (commun ément appel ée fracture de Pouteau-Colles) est fr équente. Son incidence est faible et constante avec l ’âge chez l’homme. Chez la femme, elle augmente dans l ’imm édiate postménopause et reste constante apr ès. La fracture de l’avant bras ou du poignet poignet a une valeur de signal d ’alerte car elle est tr ès pr édictive du risque ult érieur de fracture fracture : le risque de fracture de l ’extr émit é s upérieure du f émur
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Pathologie Patholo gie de l’appareil locomoteur
1
Évolution de la masse osseuse avec l’âge. l’ âge. Les courbes sont schématique schématiquess et indiquent, chez les femme femmess et les hommes, homme s, les principales principales étapes du vieillissement vieillissement osseux après l’acquisition du pic de masse osseuse. de la perte osseuse survenue par la suite (fig. 1). À partir de 35 à 40 ans, une perte osseuse dite « physiologique » survient chez l ’homme comme chez la femme. Elle est lente (0,1 à 0,5 % par an) et est attribu ée au vieillissement cellulaire osseux, en particulier des ost éoblastes, cellules charg ées de l ’ostéoformation. Dans la p ériode ménopausique (vers 50 ans), une acc élération de la perte osseuse est observée chez les femmes (1 à 3 % par an pendant les 5 à 10 ans suivant l ’arr êt des r ègles). Elle traduit une amplification de la perte osseuse lente par augmentation du remodelage osseux, directement li ée à la carence en œ strogènes. La carence œstrog énique induit une cascade de perturbations mol éculaires, modifiant la fonction des cellules osseuses : augmentation du recrutement, de l ’activité et de la dur ée de vie des ost éoclastes entra înant une augmentation de la r ésorption osseuse, et diminution de la dur é e de vie des ost é o blastes, majorant le d éficit d ’ostéoformation. La perte osseuse se ralentit à nouveau vers la soixantaine, mais se maintient à un niveau supérieur à la perte osseuse lente, et peut à nouveau s ’accélérer chez les sujets âgés. Ce phénomène est la cons équence d ’une hyperparathyroïdie secondaire à la carence calcique et vitaminique D, tr ès fr équentes apr ès 70 ans. L’excès de parathormone (PTH) augmente la r ésorption et le remodelage, particu-
2
Dé terminants terminants de la masse osseuse et de la perte osseuse. Les facte facteurs urs g é né tiques, tiques, horm hormonau onaux, x, nu nutri trition tionnels nels,, phy physiqu siques es et d ’ e environnement nvironnement d t terminent erminent la masse osseuse ( quantit ’ é é « é » ). Les alt é rations qualitatives contribuent, avec l ’ amputation é rations ’ amputation du capital osseux initial, à la fragilisation fragilisation du squelette, squelette, qui augmente le risque de fracture.
Ostéoporose cortisonique Parmi les causes identifiables d ’ostéoporose, les traitements cortisoniques prolong és sont au premier plan. Les corticoïdes retentissent pr é cocement sur les cellules osseuses, essentiellement les ost éoblastes : diminution de la prolif ération et de l ’activité ; diminution rapide de leur survie ainsi que celle des ost éocytes englobés dans la matrice osseuse. Il en r ésulte une perte osseuse rapide, mesurable d ès les premiers mois et pouvant atteindre 5 à 10 % apr ès un an de traitement cortico ïde. Son amplitude d é pend de la dose de cort ico ïdes mais est aussi tr è s variable d ’un patient à l’autre, sans facteur pr édictif. Elle est associée à une augmentation rapide du risque de fracture.
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OSTÉOPOROSE
TABLEAU III
Causes d’ostéoporoses dites « secondaires »*
A
B
C
D
Endocrinopathies
hypercorticisme et traitements cortisoniques prolong és ; hypogonadisme ; hyperparathyro ïdie ; hyperthyro hyperthyroïdie et traitements par hormones thyro ïdiennes à dose suppressive de la sécr étion de TSH ; ad énomes hypophysaires à prolactine; acrom égalie, diabète Maladies digestives
gastrectomie ; r ésections intestinales étendues; malabsorption gastrectomie malabsorption;; malnutrition,, hé patopathie malnutrition patopathiess chroniques chroniques s évères Maladies inflammatoires et systémiques
rhumatismes inflammatoires chroniques (polyarthrite rhumato ïde, spondylarthropathies) spondylarthropathies) ; infection par le virus de l’immunod éficience humaine (VIH) et traitements antir étrovira troviraux ux ; mastocytose Maladies génotypiques
maladie de Lobstein; autres maladies du tissu collagène ou du tissu élastique (maladie d ’Ehlers-Danlos, maladie de Marfan, élastorrhexie); homocystinurie homocystinurie ; hémochromatose Maladies néoplasiques
myélome multiple; cancers métastatiques; chimioth érapies anticancéreuses * Affections pouvant r éaliser une d émin minééralisation radiologique diffuse et se compliquer de fractures fractures ; elles constituent le diagnostic diff érentiel de l’ l’ ost ost éoporose primitive.
chez les hommes (60 % des ost éoporoses masculines sont « secondaires »), alors que chez la femme, l ’ostéo porose poro se dite « idiopathique » (postménopausique) est
3
Frac F racture ture-tas -tassemen sementt ost é o u éoporotique porotique d ’ ’une ne vert èbre lombaire (A, B), et tassement tassement tumoral tumoral malin au cours d ’ un myé lome lome ’ un (C,, D). Not (C Noter er le car caract act ère asymé trique trique du tassement malin sur le clich é de de face et l ’ ost é olyse du pé dicule dicule gauche (C), ’ ost é olyse ainsi que la lyse osseuse et la disparition du mur post é rieur rieur de profil (D).
idiopathique. Au contraire, une anomalie suspecte de ces examens radiologiques et biologiques simples (image de d émin éralisation lacunaire, vert è bre « borgne » p par ar effacement d ’un pédicule, vitesse de sédimentation élevée, pic monoclonal, hypercalc émie, hypophosphat émie …) doit attirer l’attention et faire demander des examens de seconde intention: intention : imagerie complémentaire (scintigraphie osseuse, tomodensitom étrie, imagerie par r ésonance magn é tique), pouvant amener à discuter une biopsie osseuse en cas de doute sur une ost éolyse tumorale, des dosages biochimiques ou hormonaux sp écialisés pour pr éciser un d ésordre phosphocalcique (ostéomalacie, hyper parathyro ïdie), une endocrinopathie (hypercorticisme, hyperthyroïdie…) ou une maladie m étabolique (hémochromatose génétique…). Les radiographies standard n ’ont pas de place pour le diagnostic d ’ost éoporose mais permettent d ’identifier ’éventuelles fractures vert é brales et doivent être faites d ’é en cas de suspicion de fracture vert é bral bralee r é cente ou ancienne.
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Pathologie Patholo gie de l’appareil locomoteur
de la perte osseuse et du risque de fracture dans des études prospectives de suivi de cohortes de femmes ménopausées. En pratique clinique, la place du dosage des marqueurs dans l ’évaluation individuelle du risque d ’ostéoporose est mal d éfinie.
T score
Traitement ✗
Moyens thérapeutiques 1. Traitement hormonal substitutif
Âge 4
Sché ma ma repr é un r é d ’ ost é odensitomé trie, trie, é sentant é sultat ’ ost é odensitom avec le c alcul du T-score. T-score.
sont mesur és : habituellement le rachis lombaire et la hanche. Par d éfaut, on peut r éaliser une mesure à l’extr émité inf érieure du radius ou sur le squelette entier, mais l’int ér êt de ces sites dans la pratique du diagnostic de l’ostéoporose n’est pas d éfini. L’interpr étation de l’examen est simple. Le r ésultat obtenu est appel é densité m min in érale osseuse et est exprim é en 2 g/cm : il s’agit en fait de la mesure de la masse min érale de l’os rapportée à l’unité de surface de la projection de la zone de mesure osseuse. Le r ésultat individuel du patient est compar compar é à la valeur moyenne m oyenne d ’une population témoin d ’adultes jeunes de même sexe et de m ême ethnie. La diff érence est exprimée en écart-type et d éfinit le T-score (fig. 4). Les sites pris en compte pour l ’interpr étation sont le rachis lombaire, le col f émoral ou la hanche totale. La valeur la plus basse est prise en consid ération pour d éfinir le statut osseux du patient : normal, ost éopénique ou ostéoporotique, selon les seuils de T-score T-score d éfinis par l’OMS. Un r écent rapport de l ’Agence nationale d ’ac’évaluation en sant é (ANAÉS) pr écise les cr éditation et d ’é
Le traitement hormonal substitutif (THS) comporte une association œstroprogestative ou une œstrogénothérapie seule. Les œstrogènes diminuent l’activité des ostéoclastes et le remodelage osseux. Ils pr éviennent la perte osseuse postm post ménopausique et peuvent augmenter la densit é minérale osseuse lombaire de 5 à 10 % chez les les femmes à distance de la m énopause. Pour pr évenir efficacement la perte osseuse acc élér ée en postménopause, le traitement œstrogénique doit être commencé pr écocement. L’action des œstrogènes d é pend de la l a dose dos e ; une dose minimale efficace sur la perte osseuse est d éfinie pour les diff érents d érivés œstrogéniques. Tous les d érivés œstrogéniques sont actifs tant que le traitement est suivi. Les modalit és pratiques sont bien codif i ées : l ’association œstroprogestative est n écessaire chez les femmes ayant leur utérus pour éviter l’hyperplasie endom étria triale le ; le schéma d ’administration peut être continu (évitant les hémorragies de privation) ou cyclique. L’efficacit é antifracturaire a été d émontr ée, essentiellement par des études é pid émiologiques d ’observation. La r éduction du risque de fracture est de l’ordre de 50 %. Elle semble semble s ’é puiser apr ès l’interruption du traitement œstrogénique, notamment pour le risque de fracture du col f émoral. La surveillance gyn écologique, particul par ticul iè rement mammaire, est capitale. L’efficacité osseuse du traitement hormonal substitutif pourrait être vérifiée d ès le 3e au 6 e mois, en dosant un marqueur du remodelage. La surveillance densitom étrique n’est pas utile tant que la femme poursuit le traitement hormonal
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OSTÉOPOROSE
2. Modu Modulateu lateurs rs sélectifs des récepteurs des œstrogènes Les « SERM » ( selective estrogen receptor modulators ) sont des molécules analogues des œstrogènes, mais de structure non stéroïdienne. En fonction des tissus cibles, ils se comportent comme des agonistes (os, système vasculaire) ou antagonistes (sein, ut érus). Le raloxif ène (Evista, Optruma) est actuellement le seul repr ésentant des SERM commercialisé pour le traitement de l ’ostéoporose postménopausique. Il diminue le remodelage osseux et pr évient la perte osseuse lombaire et f émorale chez les femmes r écemment ménopausées. Il augmente la densit é minérale osseuse lombaire et f émorale à distance de la m énopause, mais de façon moindre que le traitement hormonal substitutif. L’efficacit é antifracturaire a été évaluée dans une grande étude d ’intervention, contr ôlée contre placebo. Chez des femmes âgées en moyenne de 67 ans, le raloxif ène diminue le risque de fracture vert é brale : de 50% 50 % pour le risque de premi ère fracture vert é brale chez les femmes ayant une ost éoporose densitométrique; de 30 % pour le risque de r écidive de fracture vert é brale chez les patient patientes es ayant une ostéoporose plus sévère au d é but du traite traitement. ment. Cette étude n’a pas mis en évidence de diminution du risque de fracture non vert é brale, quel qu ’en soit le site. En France, le raloxif ène n’est rembours é que pour le traitement de l ’ost éoporose postménopausique avec ant écédent de fracture. Il est contre-indiqu é en cas de cancer du sein évolutif et d ’antécédent thromboembolique. Son action anti- œstrogénique sur le sein est en ’é valuation chez les femmes à haut risque de cours d ’é cancer. Le risque thromboembolique est augment é, de la même façon que pour le traitement hormonal substitutif. Des bouff ées de chaleur et des crampes des membres inf érieurs peuvent gêner la patiente au d é but du traite traitement. ment.
3. Bisph Bisphosph osphonat onates es Les bisphosphonates sont des analogues du pyrophosphate, à forte affinité osseuse. Ils ont une action anti-ostéoclastique et freinent puissamment et durablement le remodelage
du fait de la mauvaise absorption digestive de tous les bisphosphona bisphosp honates tes et du pote potentie ntiell d ’irritation de la muqueuse digestive des aminobisphosphonates, notamment de l’alendronate. Fosamax (10 mg/j) et Actonel (5 mg/j) doivent être pris strictement à jeun, avec un grand verre d ’eau faiblement minéralisée, sans s’allonger apr ès la prise, pour éviter tout reflux du m édicament dans l ’œsophage.
4. Mesu Mesures res diététiques et hygiène de vie Le calcium et la vitamine D sont un traitement d ’appoint classique, parfois négligé, des traitements pr écédents. La suppl émentation calcique seule est susceptible de ralentir la perte osseuse sur certains sites ou dans certains sous-groupes de patientes [femmes âgées et (ou) fortement carenc ées en calcium]. La fr équence de la carence d ’apport alimentaire en calcium a été longtemps sousestimée et justifie un d é pist pistage age par un inte interrog rrogatoi atoire re simple et la prescription d ’une supplémentation adapt ée (500 à 1 000 mg/j), en cas de carence suspect ée ou prouvée. Il en est de m ême pour la carence vitaminique D et l ’utilisation d ’un supplément par faible dose de vitamine D 3 naturelle (400 à 1 200 UI/j). La suppl émentation vitamino-calcique à dose physiologique a fait la preuve preu ve d ’une pr évention des fractures de l ’extr émit é sup érieure du f é mur dans une population de femmes âgées, carencées en calcium et en vitamine D et ayant une hyperparathyro ïdie secondaire. La diminution significative des fractures de l ’extr émité supérieure du f émur dans le groupe trait é allait de pair avec la correction de l’hyperparathyro ïdie secondaire et une augmentation significative de la densit é minérale osseuse f émorale. La sédentarité et l’absence d ’exercice physique sont des facteurs de risque d ’ostéoporose. Une activit é physique r éguli ère et une pratique sportive raisonnable sont à recommander pour leur action b énéfique osseuse, mais aussi musculaire, aidant à la pr évention des chutes. La pr évention des chutes doit être un souci constant chez les sujets âgés : correction des troubles troubles de la vision ou des troubles de l’équilibre ; limitation de la prescription de sédatifs ou d ’hypot hypotenseurs enseurs ; évaluation et correction des
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Pathologie Patholo gie de l’appareil locomoteur
2. Prévention de la perte osseuse postménopausique Elle repose essentiellement sur le traitement hormonal substitutif, à dose efficace et poursuivie suffisamment longtemps (plus de 10 ans, voire dans l ’id éal ind éfiniment). En cas de contre-indication, de refus ou d ’interruption pr ématur ée, en l’absence d ’antécédent de fracture, il convient de r éaliser une mesure de densit é min érale osseuse et une évaluation des facteurs de risque. Si le T-score est inf é rieur à – 2,5, un traitement alternatif (alendronate 5 mg, raloxif ène) sera prescrit, hors rem boursement. Si le T-score T-score est entre – 1 1 et – 2,5, 2,5, un tel traitement pourra être discuté, en fonction de la pr ésence d ’autres facteurs de risque. Ces traitements (raloxif ène, bisphosp bisp hosphonat honates) es) sero seront nt pour poursuivis suivis penda pendant nt quelq quelques ues ann ées (en moyenne 5 ans). Leur efficacit é peut être jugée sur une mesure de densit é minérale osseuse, apr ès 18 à 24 mois, ou plus rapidement (3 e-6e mois), sur une diminution du taux d ’un marqueur biochimique de la r ésorption. Apr ès 80 ans, la prescription de calcium et de vitamine D est large, et le traitement hormonal substitutif est quasi impossible ; les bisphosphonates peuvent être discutés au cas par cas.
3. Traitement de l’ostéoporose avec fractures En cas d ’antécédent de fractures ost éoporotiques, on parle de traitement « curatif », visant à pr évenir les r écidives
d ’antécédent de fracture ou pour une corticoth érapie à dose supérieure à 7,5 mg/j. En l ’absence de ces 2 cas de figure, une mesure de densit é min érale osseuse permet de guider la prescription : un T-score inf érieur ou égal à – 1,5 1,5 incite à proposer un bisphosphonate. Ce seuil est plus bas que pour l’ostéoporose postménopausique car les patients sous corticoïdes d éveloppent plus de fractures à densité minérale osseuse égale, sans doute du fait d ’altérations qualitatives osseuses, mises en évidence par des études histologiques mais non mesurables en routine. Chez les femmes non m énopaus ées et les hommes le risque est moindre, et la prescription de bisphosphonate est guid ée par le r ésultat de la densit é minérale osseuse.
5. Traitement des autres formes formes d’ostéoporose
• Les autres ’ost st é éoporoses poroses secondaires, notamautres causes d ’ o o ment les endocrinopathies, peuvent aussi b énéfic ficie ierr d ’un traitement à visée osseuse (traitement hormonal substitutif, raloxif ène, bisphosphonates), à discuter au cas par cas, en fonction du risque de fracture évalué par mesures de densité minérale osseuse. Le traitement sp écifique de la cause est aussi important et peut avoir un b énéfice osseux : la densit densité minérale osseuse r écupère ainsi une valeur normale apr ès cure chirurgicale d ’un ad énome surr énal, responsable d ’un hypercorticisme, et augmente apr ès traitement d ’une hyperparathyro ïdie primitive par ablation d ’un ad énome parathyro ïdien. • L’ ost é oporose ost é oporose masculine pose des probl èmes théra peutique peut iques, s, car car les les possib possibilit ilités sont r éduites. Il est important
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OSTÉOPOROSE
POUR APPR APPROFONDIR OFONDIR
1 / Indications de l’ostéodensitométrie pour la prise en charge de l’ostéoporose postménopausique et de l’ostéoporose cortisonique, cortisoni que, selon le rapport rapport de l’ANAES
En gras, sont indiqu indiqués les marqueurs utilisés dans la pratique clinique (les phosphatases alcalines totales sont utilis ées pour le diagnostic diff érentiel de l’ostéoporose, mais le dosage est moins sensible sensible que celui de l’iso-enzyme osseuse pour l ’évaluation des patients ostéoporotiques).
Quel que soit soit le contexte, contexte, une ostéodensitomé trie ne doit être conseillée que si le r ésultat de l’examen peut a priori conduire à une modification de la prise en charge du patient.
3 / Mesures générales de pr évention de l’ostéoporose cortisonique
Il est recommandé de réaliser une ostéodensitométrie :
◗
– devant : une fracture vertébrale non traumatique traumatique non tumorale, un ant écédent personnel de fracture périphériqu rique, e, des ant antécédents documentés de pathologies ost éopéniant niantes es ; – lors de la mise en route d’une corticothérapie systémiq mique, ue, prévue pour une durée d’au moins 3 mois cons écutifs, à une dose de 7,5 mg/j, d’équivalent prednisone. Chez la femme ménopausée, une ostéodensitométrie est : risque: antécédents de fracture – conseillée en présence de facteurs de risque: vertébrale ou du col f émoral chez un parent au 1 er degré ; en cas cas d’indice de masse corporelle < 19 kg/m2 ; en cas de ménopause avant 40 ans, ans, quell quelle e qu’en soit la cause, cause, ou de ménopause iatrogénique ; antécédent de corticothérapie prolongée (> 3 mois) mois) ; – déconseillée lorsqu’un traitement hormonal substitutif (THS) est indiqué, pre prescr scrit it à dose efficace (pour assurer une pr évention de l’ostéoporose), et bien suivi.
* http://www http://www.anaes.fr/ANAES/anaesparame .anaes.fr/ANAES/anaesparametrage.nsf/accueilnouv trage.nsf/accueilnouveautes?readform eautes?readform
◗
◗ ◗ ◗ ◗
Gestion de la corticothérapie : dose minimale minimale efficac efficace e ; durée limitée ; utilisa utilisation tion des des voies voies locales locales d’administration (aérosols, crèmes…). Correction des carences carences : traitement hormonal en cas d’hypogonadisme, essentiellement chez les femmes ménopaus ées ; supp suppllémentation vitaminocalcique physiologique. Lutte contre l’immob immobilisat ilisation, ion, l’amyotr amyotrophie ophie et l’inactivité physique Recherche et éviction des facteurs de risque associés. Évaluation du statut osseux par absorptiom étrie biphotoniqu biphotonique eà rayons X. Discussion d’un traitement par bisphospho bisphosphonate. nate.
POUR EN SAVOIR PLUS Fontana Fon tana A, Delmas PD PD. L’ostéoporose : épidémiolo miologie, gie, cliniq clinique ue et
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Gériatrie Partie I – Module 5 – Q 62
Troubles de la marche et de l’équilibre l’équilibre. Chutes chez le sujet âgé. PR F rançois PUISIEUX Service de médecine interne et gériatrie, hôpita hôpitall gériatrique les Bateliers, Bateliers, CHRU, 59000 Lille. Lille.
Points Forts à comprendre • Les troubles de la marche et de l’équilibre sont très fréquents chez le sujet âgé. • Les chutes ont des répercussions considérables en termes de santé publique. Elles sont à l’origine d’une morbidité et d’une mortalité considérables. • En dehors des conséquences traumatiques, les chutes sont souvent à l’origine d’une perte d’autonomie pouvant conduire à l’institutionnalisation. • Chez le sujet âgé, l’origine est le plus souvent
chutes, la réduction des facteurs potentiellement modifiables, l’entraînement physique et la lutte contre l’ostéoporose sont toujours nécessaires.
Épidémiologie Santé publique 1. Fréquence des troubles de la marche et de l’équilibre
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T R O U B L E S D E L A M A R C H E E T D E L’ É Q U I L IB R E . C H U T ES C H E Z L E S U J ET Â G É .
en fonction de la population étudiée. On estime qu’environ 10 % des chutes seraient responsables d’un traumatisme sans fracture justifiant un traitement médical (contusions tissulaires, traumatismes crâniens, luxations articulaires…) et 5 % seraient responsables d’une fracture. La fracture du col du fémur vient en tête ; elle représente le tiers des fractures consécutives aux chutes de la personne âgée. Les femmes (en raison de l’ostéoporose postménopausique) et les tranches d’âge les plus élevées sont les plus exposées au risque de fracture du col fémoral. Les chutes représentent près de 30 % des motifs d’hospitalisation après 65 ans. Le vieillissement de la population explique que la fréquence des chutes et, en corollaire, l’incidence de la fracture du col du fémur aient augmenté très rapidement dans nos pays au cours des 20 dernières années. L’augmentation va s’accélérer encore dans les années à venir.
3. Mortalité Les chutes sont responsables directement ou indirectement d’une importante mortalité à court terme, de l’ordre de 10 000 morts par an en France. Elles sont, de loin, la 1re cause de mortalité accidentelle chez les plus de 65 ans et seraient responsables de près de 50 % des décès par traumatisme dans cette tranche d’âge. Le risque de décès dans l’année est multiplié par 4 chez un chuteur par rapport à un non-chuteur de même âge (25 % contre 6 %). Le sexe féminin, les antécédents de chutes et le
perdre confiance en elles. Le risque est qu’elles se replient sur elles-mêmes, qu’elles réduisent leurs sorties, d’où une désinsertion sociale et un déconditionnement physique. La peur de tomber après une chute est plus fréquente chez les personnes les plus âgées et les plus fragiles et chez les femmes. La restriction d’activité paraît plus étroitement liée à la peur de tomber qu’à la chute ellemême. L’attitude protectrice de l’entourage familial contribue souvent à la perte d’autonomie. La famille en effet se propose de remplacer la personne âgée dans ses activités, notamment à l’extérieur du domicile. Comme ce qui n’est pas exercé se perd, les troubles de la marche s’aggravent, l’appréhension augmente. C’est un cercle vicieux qui s’installe. Les chutes se répètent. On dit volontiers que « la chute appelle appelle la chute ». Il peut en découler une perte d’autonomie progressive et finalement une institutionnalisation. Les études ont bien montré que la chute est une cause majeure d’entrée en institution et que ce risque est d’autant plus grand que les chutes ont été nombreuses et traumatiques.
Rappels physiologiques Fonction d’équilibre et de marche La station debout définit la posture, la fonction d’équilibration vise au maintien de celle-ci. La marche est une
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Gériatrie
modérée de l’acuité visuelle et de l’accommodation. Le vieillissement des afférences vestibulaires consiste en une diminution de la sensibilité du vestibule lors des mouvements rapides et complexes (presbyvestibulie). Il y a aussi, avec l’âge, une altération de la sensibilité proprioceptive et de la sensibilité tactile des pieds. L’âge allonge le temps de conduction nerveuse périphérique et centrale et le temps des réponses motrices. Enfin, le vieillissement s’accompagne d’une diminution de la force musculaire (sarcopénie sénile) et des amplitudes articulaires (dorsiflexion de cheville). Comme la sarcopénie est très souvent associée à l’ostéopénie, les personnes âgées sarcopéniques sont non seulement à haut risque de chutes, mais aussi à haut risque de fractures en cas de chutes. L’équilibre statique est marqué par une majoration des oscillations et une diminution des capacités à tenir la station monopodale. La marche du sujet âgé est un peu ralentie. La longueur du pas est diminuée et sa largeur augmentée. Le temps de double appui est accru au détriment de la phase d’oscillation. La posture est modifiée avec une légère flexion du tronc et de la tête. Les mouvements de balancement des membres supérieurs sont réduits.
Étape diagnostique Les chutes sont le plus souvent de mécanisme plurifactoriel. Rares sont celles qui relèvent d’une cause
pieds ; une hypotension orthostatique ; une artériopathie oblitérante des membres inférieurs ; une diminution de l’acuité visuelle ou auditive… Il faut aussi procéder à une évaluation psychique. On a déjà dit le rôle de la l a peur et des troubles thymiques dans le cercle vicieux qui peut s’installer après une chute. Chez les personnes âgées fragiles, les carences nutritionnelles étant fréquentes, il faut évaluer l’état nutritionnel.
Examen physique fonctionnel L’examen fonctionnel doit être fait dans de bonnes conditions. Les vêtements gênants doivent être retirés. L’examen se fait théoriquement pieds nus, mais il peut être utile aussi d’examiner le patient avec ses chaussures (qualité du chaussage, intérêt des talons pour corriger une rétropulsion). Il faut apprécier l’utilité des aides techniques de marche habituelles. Il faut étudier : • l’équi l’équilibre libre statiq statique ue : station assise (position des pieds et du tronc), station debout bipodale (statique du rachis, Romberg, polygone de sustentation, épreuve des poussées déséquilibrantes, réactions parachutes), station statio n monopo monopodale dale ; • l ’équilibre ’é quilibre dynamique : transferts couché-assis et assis-debout, marche sur terrain plat sur une dizaine de mètres (balancement du tronc, dissociation des ceintures, position du tronc, longueur du pas…), demi-tour, marche rapide, marche les yeux fermés,
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T R O U B L E S D E L A M A R C H E E T D E L’ É Q U I L IB R E . C H U T ES C H E Z L E S U J ET Â G É .
Chez le sujet âgé cependant, les causes sont volontiers associées et multiples et le tableau est rarement typique.
Origine polyfactorielle De très nombreuses causes individuelles peuvent altérer la marche. Ces causes dites intrinsèques peuvent être la conséquence du vieillissement lui-même mais surtout de pathologies neuromusculaires, ostéo-articulaires ou cardiovasculaires chroniques ou aiguës (qui constituent des facteurs précipitants). Les pathologies chroniques susceptibles d’altérer les performances posturo-locomotrices d’un individu sont nombreuses (tableau). Chez le sujet très âgé, habituellement polypathologique, elles sont généralement associées. Le risque de chute augmente de façon linéaire avec le nombre d’affections chroniques. La dénutrition protéino-
significative entre le risque de chute et la consommation de médicaments. Les médicaments le plus souvent en cause sont d’abord les psychotropes (antidépresseurs, sédatifs, hypnotiques, neuroleptiques), ensuite les diurétiques, les antihypertenseurs, les vasodilatateurs, les hypoglycémiants oraux, les digitaliques… La chute résulte toujours de la conjonction de 3 variables : une variable action (notion de prise de risque), une variable individu et une variable environnement. La chute survient lorsque les possibilités posturo-locomotrices d’un individu sont dépassées. Elle traduit donc un certain degré de décompensation fonctionnelle. Certaines actions sont clairement à risque. On peut déconseiller à une personne âgée de monter sur un escabeau instable pour décrocher ses rideaux. Cependant, le but du thérapeute est de maintenir l’autonomie de la personne âgée et non de restreindre ses activités.
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Gériatrie
Recherche des facteurs de risque environnementaux L’évaluation fonctionnelle se fait au mieux lors d’une visite au domicile du patient. Cette visite permet en effet de réaliser l’examen l’examen fonctionnel fonctionnel « en situation ». On peut ainsi voir comment le patient s’assoit et se relève de son propre fauteuil, comment il utilise ses WC, sa salle de bains. Chaque poste important (toilettes, cuisine, chambre…) doit être étudié. Cette visite permet de lister tous les facteurs de risque extrinsèques qui n’ont de sens que rapportés aux possibilités locomotrices du patient (par exemple, une personne malvoyante risque davantage de tomber dans un lieu mal éclairé).
Évaluation de l’autonomie
orthostatique, d’un neuroleptique orthostatique, neuroleptique utilisé utilisé « pour dormir », traitement médical ou chirurgical d’une arthrose douloureuse d’une maladie de Parkinson Parkinson ; changement de verres correcteurs ; chaussage par des chaussures chaussures tenant bien les chevilles ; aménagements de l’environnement l’environnement (rehausse du siège des WC, poignées murales, adoption de sièges hauts et fermes avec accoudoirs, chaise percée, tapis antidérapant dans la douche ou la baignoire…). Dans la plupart des cas, une rééducation est indiquée. Son objectif est de restaurer une marche de qualité (avec ou sans aide technique), sûre, c’est-à-dire sans risque de chute. La rééducation (fig. 2) est : • analytique pour corriger les déficiences (renforcement musculaire des quadriceps, assouplisse assouplissement ment articulai articu laire) re) ; • fonctionnelle : – travail de l’équilibre et des réactions d’adaptation posturale (verticalisation, équilibre du tronc lors de mouvements
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T R O U B L E S D E L A M A R C H E E T D E L’ É Q U I L IB R E . C H U T ES C H E Z L E S U J ET Â G É .
TRAVAIL D’ANTÉPULSION DU TRONC
TRAVAIL TRAV AIL AVEC AVEC BALLON : SOUPLESSE
TRAVAIL SUR TRAMPOLINE
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Gériatrie
PREMIÈRE ÉTAPE :
DEUXIÈME ÉTAPE :
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T R O U B L E S D E L A M A R C H E E T D E L’ É Q U I L IB R E . C H U T ES C H E Z L E S U J ET Â G É .
Modalités d’intervention 1. Personnes âgées en bon état de santé mais présentant une perte d’aisance locomotrice, une sensation « d’instabilité » L’expérience montre qu’un grand nombre de personnes âgées valides, vivant autonomes à leur domicile éprouvent pourtant une sensation pénible d’instabilité décrite comme une sensation vertigineuse ou de marche ébrieuse, incertaine. Ces personnes âgées sont plus que d’autres susceptibles de tomber. La gêne fonctionnelle est souvent importante mais, paradoxalement, l’examen physique analytique est pauvre et ne met pas en évidence de pathologie causale évidente. L’examen fonctionnel met en évidence une « perte d’aisance d’aisance locomotrice», caractéri caractérisée sée par une impossibilité de tenir l’équilibre lors de manœuvres
Elle intéresse aussi les responsables des institutions gériatriques et des hôpitaux, car les chutes y sont particulièrement fréquentes. Une véritable politique de prévention doit être menée dans ces ces lieux ; elle repose sur la sensibilisation du personnel au problème des chutes, sur le dépistage des sujets les plus à risque, sur l’aménagement des locaux afin de réduire au minimum les facteurs de risque environnementaux, sur la diminution de l’usage des contentions physiques (dont l’utilisation ne réduit pas le risque de chute mais favorise l’agitation et le déconditionnement des patients), sur le lever précoce des personnes âgées et leur remise à la marche systématique. Mais la prévention de la chute intéresse aussi les r esponsables politiques. Des campagnes de presse doivent être menées pour sensibiliser les personnes âgées à ce risque. Il faut aussi adapter l’urbanisme aux besoins d’une population vieillissante, ce qui passe par le maintien de
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PARTIE I / MODULE VIEILLISSEMENT
Q
61
5
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VIEILLISSEMENT
Troubles nutritionnels chez le sujet âgé Le premier examen à pratiquer est le mini nutritional assesment (MNA) qui comporte une partie de dépistage incluant les variations de poids, l’index de masse corporel (IMC) et la détermination grossière d’une anorexie. Un seuil inférieur à 12/14 indique un
des réserves nutritionnelles est plus grande chez eux que chez un adulte plus jeune. Or, le sujet âgé ne sait pas, contrairement à l’adulte jeune, reconstituer ad integrum ses réserves nutritionnelles au décours d’un syndrome inflammatoire. En effet après
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prises, ajoutée à celle de plusieurs verres d’eau pour les faire passer,, voire la modification du goût des aliments qu’elles passer entraînent en sont responsables. Le plus souvent, du moins lors des hospitalisations, il s’agit
Un IMC inférieur à 15 kg/m kg/m2 traduit une MPE majeure par insuffisance chronique d’apport, surtout si le sujet suj et est en équilibre hypométabolique (albumine corrigée corrigé e de la CRP > 35 g/L). Il a alors une atrophie de la muqueuse intestinale qui empêche une renutrition
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VIEILLISSEMENT
Troubles nutritionnels chez le sujet âgé recourir transitoirement à une insulinothérapie, beaucoup de sujets âgés tolérant mal (hyperglycémie nette) les niveaux glucidiques nécessaires. En cas de nutrition entérale, on utilise d’abord des diètes normo-
L
L
des dosages bihebdomadaires de la CRP et de la transthyrétine, de l’ionogramme sanguin (plus en cas de déséquilibre ionique) et une surveillance des points cutanés d’appui ; un dosage hebdomadaire de l’albumine et des ingesta ;
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changement d’humeur du patient et la reprise de certaines activités ; c’est pourquoi une étude quotidienne du comportement doit faire l’objet d’une attention particulière de la part du personnel soignant. Dans certains cas, souvent en cas de dépression, ces mesures
Une fois la MPE traitée et guérie, il faut prévenir sa récidive qui est fréquente, surtout en cas d’anorexie chronique. Sa prévention est une mesure de santé publique et fait partie des 9 objectifs du « Plan national nutrition santé ». Pour cela des
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